The structure of the parasympathetic nervous system. Parasympathetic Nervous System Location of the Parasympathetic Nervous System

The ANS is divided into two divisions - sympathetic and parasympathetic. In structure, they differ in the location of their central and effector neurons, their reflex arcs. They also differ in their influence on the functions of innervated structures.

What are the differences between these departments? The central neurons of the sympathetic nervous system are usually located in the gray matter of the lateral horns. spinal cord from 8 cervical to 2-3 lumbar segments. Thus, sympathetic nerves always depart only from the spinal cord as part of spinal nerves along the anterior (ventral) roots.

The central neurons of the parasympathetic nervous system are located in the sacral segments of the spinal cord (segments 2-4), but most of the central neurons are in the brain stem. Most of the nerves of the parasympathetic system depart from the brain as part of the mixed cranial nerves. Namely: from the midbrain as part of the III pair (oculomotor nerve) - innervating the muscles of the ciliary body and the annular muscles of the pupil of the eye, the facial nerve comes out of the Varolii bridge - VII pair (secretory nerve) innervates the glands of the nasal mucosa, lacrimal glands, submandibular and sublingual glands. From medulla oblongata IX pair departs - secretory, glossopharyngeal nerve, innervates the parotid salivary glands and glands of the mucous membranes of the cheeks and lips, X pair ( nervus vagus) - the most significant part of the parasympathetic division of the ANS, passing into the chest and abdominal cavities, innervates the entire complex of internal organs. Nerves extending from the sacral segments (segments 2-4) innervate the pelvic organs and are part of the hypogastric plexus.

The effector neurons of the sympathetic nervous system are located on the periphery and are located either in the paravertebral ganglia (in the sympathetic nerve chain) or prevertebral. Postganglionic fibers form various plexuses. Among them, the most importance has a celiac (solar) plexus, but it includes not only sympathetic, but also parasympathetic fibers. It provides innervation to all organs located in abdominal cavity. That is why blows and injuries to the upper part of the abdominal cavity (approximately under the diaphragm) are so dangerous. They are able to evoke state of shock.

The effector neurons of the parasympathetic nervous system are always located in the walls of the internal organs (intramurally). Thus, in parasympathetic nerves, most of the fibers are covered myelin sheath, and the impulses reach the effector organs faster than those of the sympathetic. This provides parasympathetic nerve influences that ensure the conservation of the resources of the organ and the organism as a whole. The internal organs located in the chest and abdominal cavity are innervated mainly by the vagus nerve (n. vagus), so these influences are often called vagal (vagal).

There are significant differences in their functional characteristics.

The sympathetic department, as a rule, mobilizes the body's resources for energetic activity (the work of the heart increases, the lumen of the blood vessels narrows and blood pressure rises, breathing quickens, pupils dilate, etc.), but the work slows down digestive systems s, with the exception of the work of the salivary glands. In animals, this always happens (they need saliva to lick possible wounds), but in some people, when excited, salivation increases.

Parasympathetic, on the contrary, stimulates the digestive system. It is no coincidence that after a hearty meal lethargy is noted, we want to sleep so much. Upon stimulation of the parasympathetic nervous system ensures the restoration of the balance of the internal environment of the body. It ensures the work of internal organs at rest.

In a functional sense, the sympathetic and parasympathetic systems are antagonists, complementing each other in the process of maintaining homeostasis, so many organs receive dual innervation - both from the sympathetic and parasympathetic departments. But, as a rule, either one or the other department of the ANS predominates in different people. It is no coincidence that the famous Russian physiologist L.A. Orbeli tried to classify people on this basis. He identified three types of people: sympathicotonic (with a predominance of the tone of the sympathetic nervous system) - they are distinguished by dry skin, increased excitability; the second type - vagotonics with a predominance of parasympathetic influences - is characteristic of them oily skin, delayed reactions. The third type is intermediate. From everyday practice, each of us can notice that tea and coffee cause different reactions in people with different type functional activity of the ANS. From animal experiments it is known that in animals with different types of ANS, the administration of bromine and caffeine also has different reactions. But throughout a person's life, their type of ANS can change depending on age, puberty, pregnancy, and other influences. Despite these differences, both of these systems, however, constitute a single functional whole, since the integration of their functions is carried out at the level of the central nervous system. In the gray matter of the spinal cord, the centers of autonomic and somatic reflexes successfully coexist, just as they are located close to each other in the brain stem, and in higher subcortical centers. Just as, ultimately, the entire nervous system functions in unity.

Functional maturation of the peripheral parts of the autonomic nervous system is closely related to the state of the higher parts of the central nervous system; after birth, in the early stages of postnatal ontogenesis, the centers of the sympathetic nervous system are mainly regulated. The tone of the parasympathetic system, in particular the vagus nerve, is absent. The vagus nerve is included in the reflex reactions at the 2-3rd month of a child's life. At the same time, the divisions of the autonomic nervous system begin to function in different dates ontogenesis is not the same in relation to different organs and systems. So, with respect to the digestive organs, the parasympathetic system first turns on, and sympathetic regulation begins to act during the period of weaning the baby from the breast. Regarding the regulation of the activity of the heart, the sympathetic system is activated before the vagal one. As the results show experimental studies, transfer of excitation to autonomic ganglia in newborns, it is carried out by the adrenergic route, and not with the help of acetylcholine, as is observed in adults.

Thus, sympathetic transmission of excitation during early ontogenesis is characterized by a large number of adrenergic synapses. In old age, sympathetic and parasympathetic tonic influences on the activity of a number of organs weaken. This affects the course of important vegetative reactions and metabolic processes and thereby limits the adaptive capabilities of an aging organism. Along with this, in the process of aging, the content of catecholamines in the blood decreases, but the sensitivity of cells and tissues to their actions, as well as to a number of other physiological changes, increases. active substances. The weakening of vegetative reactions is one of the reasons for the decline in working capacity during aging.

During the aging period, structural and functional disorders occur in the autonomic ganglia, which can prevent the transmission of impulses to them and affect the trophism of the tissue that is innervated. The hypothalamic regulation of vegetative functions changes significantly, which is an important mechanism of body aging.

Projections of autonomic centers are also presented in the cerebral cortex - mainly in the limbic and rostral parts of the cortex. Parasympathetic and sympathetic projections of the same organs are projected to the same or closely located areas of the cortex, this is understandable, since they jointly provide the functions of these organs. It has been established that parasympathetic projections in the cortex are much wider than sympathetic ones, however, functionally sympathetic influences are longer than parasympathetic ones. This is due to differences in mediators that are released by the endings of sympathetic (adrenaline and norepinephrine) and parasympathetic (acetylcholine) fibers. Acetylcholine, a mediator of the parasympathetic system, is quickly inactivated by the enzyme acetylcholinesterase (cholinesterase) and its effects quickly disappear, while adrenaline and norepinephrine are inactivated much more slowly (by the enzyme monoamine oxidase), their effect is enhanced by norepinephrine and adrenaline secreted by the adrenal glands. Thus, sympathetic influences last longer and are more pronounced than parasympathetic ones. However, during sleep, parasympathetic influences on all our functions prevail, which helps to restore the body's resources.

The autonomic nervous system carries out two kinds of reflexes: functional and trophic.

The functional effect on the organs is that irritation autonomic nerves either calls the function of the organ, or slows it down (the "starting" function).

The trophic influence consists in the fact that the metabolism in the organs is directly regulated and thereby the level of their activity is determined (the “corrective” function).

Vegetative reflexes are usually divided into:

  • 1) viscero-visceral, when both afferent and efferent links, i.e. the beginning and effect of the reflex refers to the internal organs or the internal environment (gastro-duodenal, gastrocardial, angiocardial, etc.);
  • 2) viscero-somatic, when a reflex starting with irritation of interoceptors due to associative connections nerve centers realized as a somatic effect. For example, when the chemoreceptors of the carotid sinus are irritated by an excess of carbon dioxide, the activity of the respiratory intercostal muscles increases and breathing becomes more frequent;
  • 3) viscero-sensory, - a change in sensory information from exteroceptors when the interoceptors are stimulated. For example, when oxygen starvation myocardium, there are so-called reflected pains in areas of the skin (Head's zones) that receive sensory conductors from the same segments of the spinal cord;
  • 4) somato-visceral, when the vegetative reflex is realized upon stimulation of the afferent inputs of the somatic reflex. For example, during thermal irritation of the skin, the skin vessels expand and the vessels of the abdominal organs narrow. Somato-vegetative reflexes also include the Ashner-Dagnini reflex - a decrease in the pulse with pressure on the eyeballs.

Reflexes of the autonomic nervous system (sympathetic and parasympathetic) can be conditionally divided into skin-vascular reflexes, visceral reflexes, pupillary reflexes.

The ANS is divided into two divisions sympathetic and parasympathetic. In structure, they differ in the location of their central and effector neurons, their reflex arcs. They also differ in their influence on the functions of innervated structures.

What are the differences between these departments?

The central neurons of the sympathetic nervous system are located, as a rule, in the gray matter of the lateral horns of the spinal cord from 8 cervical to 2-3 lumbar segments. Thus, sympathetic nerves always depart only from the spinal cord as part of the spinal nerves along the anterior (ventral) roots.

The central neurons of the parasympathetic nervous system are located in the sacral segments of the spinal cord (segments 2-4), but most of the central neurons are in the brain stem. Most of the nerves of the parasympathetic system depart from the brain as part of the mixed cranial nerves. Namely: from the midbrain as part of the III pair (oculomotor nerve) - innervating the muscles of the ciliary body and the annular muscles of the pupil of the eye, the facial nerve comes out of the Varolian bridge - VII pair (secretory nerve) innervates the glands of the nasal mucosa, lacrimal glands, submandibular and sublingual glands. The IX pair departs from the medulla oblongata - the secretory, glossopharyngeal nerve, innervates the parotid salivary glands and glands of the mucous membrane of the cheeks and lips, the X pair (vagus nerve) - the most significant part of the parasympathetic division of the ANS, passing into the chest and abdominal cavities, innervates the entire complex of internal organs. Nerves extending from the sacral segments (segments 2-4) innervate the pelvic organs and are part of the hypogastric plexus.

The effector neurons of the sympathetic nervous system are located on the periphery and are located either in the paravertebral ganglia (in the sympathetic nerve chain) or prevertebral. Postganglionic fibers form various plexuses. Among them, the most important is the celiac (solar) plexus, but it includes not only sympathetic, but also parasympathetic fibers. It provides innervation to all organs located in the abdominal cavity. That is why blows and injuries to the upper part of the abdominal cavity (approximately under the diaphragm) are so dangerous. They can cause shock. Effector neurons of the parasympathetic nervous system always located in the walls of internal organs (intramurally). Thus, in the parasympathetic nerves, most of the fibers are covered with a myelin sheath, and the impulses reach the effector organs faster than in the sympathetic one. This provides parasympathetic nerve influences that ensure the conservation of the resources of the organ and the organism as a whole. The internal organs located in the chest and abdominal cavity are innervated mainly by the vagus nerve (n.vagus), so these influences are often called vagal (vagal).


There are significant differences in their functional characteristics.

The sympathetic department, as a rule, mobilizes the resources of the body for energetic activity (the work of the heart increases, the lumen of the blood vessels narrows and blood pressure rises, breathing quickens, pupils dilate, etc.), but the digestive system is inhibited, with the exception of the work of the salivary glands. In animals, this always happens (they need saliva to lick possible wounds), but in some people, when excited, salivation increases.

Parasympathetic, on the contrary, stimulates the digestive system. It is no coincidence that after a hearty meal lethargy is noted, we want to sleep so much. When excited, the parasympathetic nervous system ensures the restoration of the balance of the internal environment of the body. It ensures the work of internal organs at rest.

In a functional sense, the sympathetic and parasympathetic systems are antagonists, complementing each other in the process of maintaining homeostasis, so many organs receive dual innervation - both from the sympathetic and parasympathetic departments. But, as a rule, either one or the other department of the ANS predominates in different people. It is no coincidence that the famous Russian physiologist L.A. Orbeli tried to classify people on this basis. He identified three types of people: sympathicotonic(with a predominance of the tone of the sympathetic nervous system) - they are distinguished by dry skin, increased excitability; second type - vagotonics with a predominance of parasympathetic influences - they are characterized by oily skin, slow reactions. The third type - intermediate. L.A. Orbeli considered knowledge of these types important for physicians, especially when prescribing doses. medicines, since the same drugs in the same dose have different effects on patients with different types of ANS. Even from everyday practice, each of us can notice that tea and coffee cause different reactions in people with different types of ANS functional activity. From animal experiments it is known that in animals with different types of ANS, the administration of bromine and caffeine also has different reactions. But throughout a person's life, their type of ANS can change depending on age, puberty, pregnancy, and other influences. Despite these differences, both of these systems, however, constitute a single functional whole, since the integration of their functions is carried out at the level of the central nervous system. You already know that in the gray matter of the spinal cord, the centers of vegetative and somatic reflexes successfully coexist, just as they are located close to each other in the brain stem and in higher subcortical centers. Just as, ultimately, the entire nervous system functions in unity.

The subcortical higher centers of the ANS are located in the hypothalamus, which is connected by extensive nerve connections with other parts of the CNS. The hypothalamus is also part of the limbic system of the brain. The functions of the autonomic nervous system, as is known, are not controlled by human consciousness. But it is through the hypothalamus and (the pituitary gland associated with it) that the higher parts of the central nervous system are able to influence the functional activity of the autonomic nervous system and through it the functions of internal organs. The functions of the respiratory, cardiovascular, digestive and other organ systems are directly regulated by autonomic centers located in the middle, oblong sections of the brain and spinal cord, which are subordinate in their functions to the centers of the hypothalamus. At the same time, the nuclei of the black substance continue there, the black nuclei located in the midbrain, the reticular formation. Indeed, the realization of the influence of a person’s mental reactions on somatic ones is an increase blood pressure with anger, increased sweating with fear, dry mouth with excitement and many other manifestations of mental conditions - occurs with the participation of the hypothalamus and ANS under the influence of the cerebral cortex.

The hypothalamus is part of the diencephalon. It can highlight anterior section(anterior hypothalamus) and posterior (posterior hypothalamus). Numerous clusters are located in the hypothalamus gray matter- cores. There are more than 32 pairs. According to their location, they are divided into areas - preoptic, anterior, middle and posterior. Each of these areas contains groups of nuclei responsible for the autonomic regulation of functions, as well as nuclei that secrete neurohormones. These nuclei are also distinguished by their functions. So, in the anterior region there are nuclei that perform the functions of regulating heat transfer due to the expansion of blood vessels and an increase in sweat separation. And the nuclei that regulate heat production (due to increased catabolic reactions and involuntary muscle contractions) are located in the posterior region of the hypothalamus. In the hypothalamus there are centers for the regulation of all types of metabolism - protein, fat, carbohydrate, centers of hunger and satiety. Among the groups of nuclei of the hypothalamus are the centers of regulation of water-salt metabolism, associated with the center of thirst, which forms the motivation for the search and consumption of water.

In the anterior region of the hypothalamus, there are nuclei involved in the regulation of the alternation of sleep and wakefulness (circadian rhythms), as well as in the regulation of sexual behavior.

Projections of autonomic centers are also presented in the cerebral cortex - mainly in the limbic and rostral parts of the cortex. Parasympathetic and sympathetic projections of the same organs are projected to the same or closely located areas of the cortex, this is understandable, since they jointly provide the functions of these organs. It has been established that parasympathetic projections in the cortex are much wider than sympathetic ones, however, functionally sympathetic influences are longer than parasympathetic ones. It has to do with differences mediators, which are released by the endings of sympathetic (adrenaline and norepinephrine) and parasympathetic (acetylcholine) fibers. Acetylcholine, a mediator of the parasympathetic system, is quickly inactivated by the enzyme acetylcholinesterase (cholinesterase) and its effects quickly disappear, while adrenaline and norepinephrine are inactivated much more slowly (by the enzyme monoamine oxidase), their effect is enhanced by norepinephrine and adrenaline secreted by the adrenal glands. Thus, sympathetic influences last longer and are more pronounced than parasympathetic ones. However, during sleep, parasympathetic influences on all our functions prevail, which helps to restore the body's resources.

But, despite the differences in the structure and functions of the various parts of the ANS, the differences in the somatic and autonomic systems, in the end, the entire nervous system works as a whole and integration occurs at all levels of both the spinal cord and the brain. And the highest level of integration, of course, is the cerebral cortex, which combines both our motor activity, the work of our internal organs and, ultimately, all human mental activity.

18. Physiology of the adrenal glands, the role of their hormones in the regulation of body functions, the relationship with other regulatory mechanisms.

Acetylcholine. Acetylcholine serves as a neurotransmitter in all autonomic ganglia, in postganglionic parasympathetic nerve endings, and in postganglionic sympathetic nerve endings innervating the exocrine sweat glands. The enzyme choline acetyltransferase catalyzes the synthesis of acetylcholine from acetyl CoA produced in nerve endings and from choline actively absorbed from the extracellular fluid. Within cholinergic nerve endings, stores of acetylcholine are stored in discrete synaptic vesicles and released in response to nerve impulses that depolarize nerve endings and increase calcium entry into the cell.

cholinergic receptors. Various receptors for acetylcholine exist on postganglionic neurons in autonomic ganglia and in postsynaptic autonomic effectors. Receptors located in the autonomic ganglia and in the adrenal medulla are stimulated mainly by nicotine (nicotinic receptors), while those located in the autonomic cells of the effector organs are stimulated by the alkaloid muscarine (muscarinic receptors). Ganglion blockers act against nicotinic receptors, while atropine blocks muscarinic receptors. Muscarinic (M) receptors are classified into two types. Mi receptors are localized in the central nervous system and, possibly, in the parasympathetic ganglia; M2 receptors are non-neuronal muscarinic receptors located on smooth muscle, myocardium, and glandular epithelium. The selective agonist of M 2 receptors is bnechol; Pirenzepine being tested is a selective M 1 receptor antagonist. This drug causes a significant decrease in secretion gastric juice. Phosphatidylinositol and inhibition of adenylate cyclase activity can serve as other mediators of muscarinic effects.

Acetylcholinesterase. Hydrolysis of acetylcholine by acetylcholinesterase inactivates this neurotransmitter at cholinergic synapses. This enzyme (also known as specific or true cholinesterase) is present in neurons and is distinct from butyrocholinesterase (serum cholinesterase or pseudocholinesterase). The latter enzyme is present in plasma and non-neuronal tissues and does not play a primary role in terminating the action of acetylchiline in autonomic effectors. Pharmacological effects anticholinesterase agents are due to inhibition of neural (true) acetylcholinesterase.

Physiology of the parasympathetic nervous system. The parasympathetic nervous system is involved in the regulation of the functions of the cardiovascular system, the digestive tract, and the genitourinary system. Tissues in organs such as the liver, kidneys, pancreas, and thyroid also have parasympathetic innervation, suggesting that the parasympathetic nervous system is also involved in metabolic regulation, although the cholinergic effect on metabolism is not well characterized.



The cardiovascular system. The parasympathetic effect on the heart is mediated through the vagus nerve. Acetylcholine reduces the rate of spontaneous depolarization of the sinoatrial node and reduces the heart rate. Heart rate under various physiological conditions is the result of a coordinated interaction between sympathetic stimulation, parasympathetic inhibition, and automatic activity of the sinoatrial pacemaker. Acetylcholine also delays conduction of excitation in the atrial muscles while shortening the effective refractory period; this combination of factors can cause the development or permanent persistence of atrial arrhythmias. In the atrioventricular node, it reduces the rate of conduction of excitation, increases the duration of the effective refractory period, and thereby weakens the response of the ventricles of the heart during atrial flutter or fibrillation (chapter 184). The weakening of the inotropic action caused by acetylcholine is associated with presynaptic inhibition of sympathetic nerve endings, as well as with a direct inhibitory effect on the atrial myocardium. The ventricular myocardium is less affected by acetylcholine, since its innervation by cholinergic fibers is minimal. A direct cholinergic effect on the regulation of peripheral resistance seems unlikely due to the weak parasympathetic innervation of the peripheral vessels. However, the parasympathetic nervous system can influence peripheral resistance indirectly by inhibiting the release of norepinephrine from sympathetic nerves.

Digestive tract. Parasympathetic innervation of the intestines is carried out through the vagus nerve and the pelvic sacral nerves. The parasympathetic nervous system increases the tone of the smooth muscles of the digestive tract, relaxes the sphincters, and increases peristalsis. Acetylcholine stimulates exogenous secretion of gastrin, secretin and insulin by the epithelium.

Urogenital and respiratory system. The sacral parasympathetic nerves innervate the bladder and genital organs. Acetylcholine increases peristalsis of the ureters, causes muscle contraction Bladder, carrying out its emptying, and relaxes the urogenital diaphragm and the sphincter of the bladder, thereby playing a major role in coordinating the process of urination. The airways are innervated by parasympathetic fibers from the vagus nerve. Acetylcholine increases secretion in the trachea and bronchi and stimulates bronchospasm.

Pharmacology of the parasympathetic nervous system. Cholinergic agonists. The therapeutic value of acetylcholine is small due to the wide dispersion of its effects and the short duration of action. Substances homogeneous with it are less sensitive to hydrolysis by cholinesterase and have a narrower range of physiological effects. bnechol, the only systemic cholinergic agonist used in daily practice, stimulates the smooth muscles of the digestive tract and urinary tract. with minimal impact on cardiovascular system. It is used in the treatment of urinary retention in the absence of urinary tract obstruction, and less frequently in the treatment of disorders of the digestive tract, such as gastric atony after vagotomy. Pilocarpine and carbachol are cholinergic agonists local action used to treat glaucoma.

Acetylcholinesterase inhibitors. Cholinesterase inhibitors enhance the effects of parasympathetic stimulation by reducing the inactivation of acetylcholine. The therapeutic value of reversible cholinesterase inhibitors depends on the role of acetylcholine as a neurotransmitter in skeletal muscle synapses between neurons and effector cells and in the central nervous system and includes the treatment of myasthenia gravis (chap. 358), cessation of neuromuscular blockade that has developed after anesthesia, and reversal intoxication caused by substances with central anticholinergic activity. Physostigmine, which is a tertiary amine, readily penetrates the central nervous system, while related quaternary amines [proserine, pyridostigmine bromide, oxazil, and edrophonium (Edrophonium)] do not. Organophosphorus cholinesterase inhibitors cause irreversible blockade of cholinesterase; these substances are mainly used as insecticides and are of primary toxicological interest. In the autonomic nervous system, cholinesterase inhibitors are of limited use in the treatment of intestinal and bladder smooth muscle dysfunction (eg, paralytic ileus and bladder atony). Cholinesterase inhibitors cause a vagotonic reaction in the heart and can be effectively used to stop attacks of paroxysmal supraventricular tachycardia (chap. 184).

Substances that block cholinergic receptors. Atropine blocks muscarinic cholinergic receptors and has little effect on cholinergic neurotransmission in autonomic ganglia and neuromuscular junctions. Many effects of atropine and atropine-like drugs on the central nervous system can be attributed to blockade of the central muscarinic synapses. The homogeneous alkaloid scopolamine is similar in its action to atropine, but causes drowsiness, euphoria and amnesia - effects that allow it to be used for premedication before anesthesia.

Atropine increases heart rate and increases atrioventricular conduction; this makes it useful in the treatment of bradycardia or heart block associated with increased vagal tone. In addition, atropine relieves bronchospasm mediated through cholinergic receptors and reduces secretion in respiratory tract, which allows it to be used for premedication before anesthesia.

Atropine also reduces the peristalsis of the digestive tract and secretion in it. Although various atropine derivatives and related substances [eg, propaneline (Propantheline), isopropamide (Isopropamide) and glycopyrrolate (Glycopyrrolate)] have been promoted as treatments for patients suffering from stomach ulcers or diarrheal syndrome, long-term use of these drugs is limited to such manifestations of parasympathetic oppression, like dry mouth and urinary retention. Pirenzepine, a trial selective Mi-inhibitor, inhibits gastric secretion, used at doses that have minimal anticholinergic effects in other organs and tissues; this drug may be effective in the treatment of stomach ulcers. When inhaled, atropine and its related substance ipratropium (Ipratropium) cause bronchial dilatation; they have been used in experiments to treat bronchial asthma.

CHAPTER 67. ADENYLATE CYCLASE SYSTEM

Henry R. Bourne

Cyclic 3`5`-monophosphate (cyclic AMP) acts as an intracellular secondary mediator for a variety of peptide hormones and biogenic amines, drugs and toxins. Therefore, the study of the adenylate cyclase system is essential for understanding the pathophysiology and treatment of many diseases. Investigation of the role of the secondary mediator of cyclic AMP has expanded our knowledge of endocrine, nervous, and cardiovascular regulation. Conversely, research aimed at unraveling the biochemical basis of certain diseases has contributed to the understanding of the molecular mechanisms that regulate the synthesis of cyclic AMP.

Biochemistry. The sequence of action of enzymes involved in the implementation of the effects of hormones (primary mediators) through cyclic AMP is shown in Fig. 67-1, and a list of hormones acting through this mechanism is given in table. 67-1. The activity of these hormones is initiated by their binding to specific receptors located on the outer surface of the plasma membrane. The hormone-receptor complex activates the membrane-bound enzyme adenylate cyclase, which synthesizes cyclic AMP from intracellular ATP. Within the cell, cyclic AMP relays information from the hormone by binding to its own receptor and activating this cyclic AMP receptor-dependent protein kinase. An activated protein kinase transfers the terminal phosphorus of ATP to specific protein substrates (usually enzymes). Phosphorylation of these enzymes enhances (or in some cases inhibits) their catalytic activity. The altered activity of these enzymes causes the characteristic action of a certain hormone on its target cell.

The second class of hormones act by binding to membrane receptors that inhibit adenylate cyclase. The action of these hormones, designated Hi, in contrast to stimulatory hormones (He), is described in more detail below. On fig. 67-1 also shows additional biochemical mechanisms that limit the action of cyclic AMP. These mechanisms can also be regulated with the participation of hormones. This allows for fine-tuning of cell function through additional neural and endocrine mechanisms.

Biological role cyclic AMP. Each of the protein molecules involved in the complex mechanisms of stimulation - inhibition, presented in Fig. 67-1, is a potential site for regulating the hormonal response to the therapeutic and toxic effects of drugs and to pathological changes occurring during the course of the disease. Specific examples of such interactions are discussed in later sections of this chapter. To bring them together, it is necessary to consider the general biological functions of AMP as a secondary mediator, which is advisable to do on the example of the regulation of the release of glucose from glycogen stores contained in the liver (the biochemical system in which cyclic AMP was found) with the help of glucagon and other hormones.

Rice. 67-1. Cyclic AMP is a secondary intracellular mediator for hormones.

The figure shows an ideal cell containing protein molecules (enzymes) involved in the mediator actions of hormones carried out through cyclic AMP. The black arrows indicate the flow of information from the stimulating hormone (He) to the cellular response, while the light arrows indicate the direction of the opposite processes, modulating or inhibiting the flow of information. Extracellular hormones stimulate (He) or inhibit (Hi) the membrane enzyme adenylate cyclase (AC) (see description in text and Fig. 67-2). AC converts ATP to cyclic AMP (cAMP) and pyrophosphate (PPI). The intracellular concentration of cyclic AMP depends on the ratio between the rate of its synthesis and the characteristics of two other processes aimed at removing it from the cell: cleavage by cyclic nucleotide phosphodiesterase (PDE), which converts cyclic AMP into 5 "-AMP, and removal from the cell by energy-dependent transport The intracellular effects of cyclic AMP are mediated or regulated by at least five additional classes of proteins.The first of these, cAMP-dependent protein kinase (PK), consists of regulatory (P) and catalytic (K) subunits.In the holoenzyme of PK, the K subunit is catalytically inactive ( is inhibited by the P subunit.) Cyclic AMP acts by binding to the P subunits, releasing the K subunits from the cAMP-P complex. (S~F) these protein substr ates (usually enzymes) initiate the characteristic effects of cyclic AMP within the cell (eg, activation of glycogen phosphorylase, inhibition of glycogen synthetase). The proportion of kinase protein substrates in the phosphorylated state (C-P) is regulated by two additional classes of proteins: kinase-inhibiting protein (IKP) reversibly binds to K-K, making it catalytically inactive (K-KP) Phosphatases (P-ase) convert S-P back to C, taking away the covalently bound phosphorus.

Transfer of hormonal signals across the plasma membrane. The biological stability and structural complexity of peptide hormones like glucagon make them carriers of diverse hormonal signals between cells, but impair their ability to cross cell membranes. Hormone-sensitive adenylate cyclase allows the information content of the hormonal signal to penetrate the membrane, although the hormone itself cannot penetrate it.

Table 67-1. Hormones for which cyclic AMP serves as a secondary mediator

Hormone Target:organ/tissue Typical action
adrenocorticotropic hormone Adrenal cortex Cortisol production
Calcitonin Bones Serum calcium concentration
Catecholamines (b-adrenergic) Heart Heart rate, myocardial contractility
Chorionic gonadotropin Ovaries, testes Production of sex hormones
Follicle-stimulating hormone Ovaries, testes Gametogenesis
Glucagon Liver Glycogenolysis, release of glucose
luteinizing hormone Ovaries, testes \ Production of sex hormones
luteinizing hormone releasing factor Pituitary f Release of luteinizing hormone
Melanocyte-stimulating hormone skin (melanocytes) T Pigmentation
parathyroid hormone Bones, kidneys T Serum calcium concentration [serum phosphorus concentration
Prostacyclin, prosta-glandin e | platelets [ Platelet aggregation
Thyroid-stimulating hormone Thyroid T Production and release of Tz and T4
thyroid-stimulating hormone releasing factor Pituitary f Release of thyroid-stimulating hormone
Vasopressin kidneys f Urine concentration

Note. Only the most convincingly documented effects mediated by cyclic AMP are listed here, although many of these hormones exhibit multiple actions in various target organs.

Gain. By binding to a small number of specific receptors (probably less than 1000 per cell), glucagon stimulates the synthesis of a much larger number of cyclic AMP molecules. These molecules in turn stimulate cyclic AMP-dependent protein kinase, which causes the activation of thousands of molecules of hepatic phosphorylase (an enzyme that limits the breakdown of glycogen) and the subsequent release of millions of glucose molecules from a single cell.

Metabolic coordination at the level of a single cell. In addition to cyclic AMP-mediated protein phosphorylation stimulating phosphorylase and promoting the conversion of glycogen to glucose, this process simultaneously deactivates the enzyme that synthesizes glycogen (glycogen synthetase) and stimulates enzymes that cause gluconeogenesis in the liver. Thus, a single chemical signal - glucagon - mobilizes energy reserves through several metabolic pathways.

Transformation of various signals into a single metabolic program. Because hepatic adenylyl cyclase can be stimulated by epinephrine (acting through β-adrenergic receptors) as well as by glucagon, cyclic AMP allows two hormones with different chemical structures to regulate carbohydrate metabolism in the liver. If there were no secondary mediator, then each of the regulatory enzymes involved in the mobilization of hepatic carbohydrates would have to be able to recognize both glucagon and adrenaline.

Rice. 67-2. Molecular mechanism of regulation of cyclic AMP synthesis by hormones, hormone receptors and G-proteins. Adenylate cyclase (AC) in its active form(AC+) converts ATP into cyclic AMP (cAMP) and pyrophosphate (PFi). Activation and inhibition of AC are mediated by formally identical systems shown on the left and right sides of the figure. In each of these systems, the G-protein fluctuates between an inactive state, being associated with GDP (G-GDP), and an active state, being associated with GTP (G 4 "-GTP); only proteins that are in an active state can stimulate ( Gs) or inhibit (GI) AC activity. Each G-GTP complex has an intrinsic GTPase activity that converts it to an inactive G-GDP complex. To return the G-protein to its active state, stimulating or inhibiting hormone-receptor complexes (HcRc and NiRi, respectively) contribute to the replacement of GDP by GTP at the site of binding of the G-protein to the guanine nucleotide.While the HyR complex is required for the initial stimulation or inhibition of AC by Gs or Hz proteins, the hormone can detach from the receptor, regardless of the regulation of AC, which, on the contrary, depends on the duration of the binding state between GTP and the corresponding G-protein, regulated by its internal GTPase.Two bacterial toxins regulate the activity of adenylate cyclase by catalyzing ADP-ribose ylation of G-proteins (see. text). ADP-ribosylation of G with cholera toxin inhibits the activity of its GTPases, stabilizing Gs in its active state and thereby increasing the synthesis of cyclic AMP. In contrast, ADP-ribosylation of Hy by pertussis toxin prevents its interaction with the gniri complex and stabilizes Hy in the inactive state bound to GDP; as a result, pertussis toxin prevents hormonal inhibition of AC.

Coordinated regulation of various cells and tissues by a primary mediator. In the classic fight-or-flight stress response, catecholamines bind to β-adrenergic receptors located in the heart, adipose tissue, blood vessels, and many other tissues and organs, including the liver. If cyclic AMP did not mediate most of the responses to the action of b-adrenergic catecholamines (for example, an increase in heart rate and myocardial contractility, dilation of blood vessels supplying blood to skeletal muscles, mobilization of energy from carbohydrate and fat stores), then the combination of a huge number of individual enzymes in tissues would have to have specific binding sites for regulation by catecholamines.

Similar examples of the biological functions of cyclic AMP could be given in relation to other primary mediators shown in Table. 67-1. Cyclic AMP acts as an intracellular mediator for each of these hormones, indicating their presence on the cell surface. Like all efficient mediators, cyclic AMP provides a simple, economical, and highly specialized pathway for the transmission of heterogeneous and complex signals.

Hormone sensitive adenylate cyclase. The main enzyme mediating the corresponding effects of this system is Hormone-sensitive adenylate cyclase. This enzyme consists of at least five classes of separable proteins, each of which is embedded in the adipose bilayer plasma membrane (Fig. 67-2).

Two classes of hormone receptors, Pc and Pu, are found on the outer surface of the cell membrane. They contain specific recognition sites for binding hormones that stimulate (Hc) or inhibit (Hi) adenylate cyclase.

The catalytic element adenylate cyclase (AC), found on the cytoplasmic surface of the plasma membrane, converts intracellular ATP into cyclic AMP and pyrophosphate. Two classes of guanine nucleotide-binding regulatory proteins are also present on the cytoplasmic surface. These proteins, Gs and Gi, mediate the stimulatory and inhibitory effects perceived by the Pc and Pu receptors, respectively.

Both stimulating and inhibitory pair functions of proteins depend on their ability to bind guanosine triphosphate (GTP) (see Fig. 67-2). Only GTP-bound forms of G-proteins regulate the synthesis of cyclic AMP. Neither stimulation nor inhibition of AC is a permanent process; instead, the terminal phosphorus of the GTP in each G-GTP complex is eventually hydrolyzed, and the Gs-GDP or Gi-GDP cannot regulate AC. For this reason, persistent processes of stimulation or inhibition of adenylate cyclase require continuous conversion of G-GDP to G-GTP. In both pathways, hormone-receptor complexes (HcRc or NiRi) enhance the conversion of GDP to GTP. This temporally and spatially recirculating process separates the binding of hormones to receptors from the regulation of cyclic AMP synthesis, using energy reserves in the terminal phosphorus bond of GTP to enhance the action of hormone-receptor complexes.

This diagram explains how several different hormones can stimulate or inhibit the synthesis of cyclic AMP within a single cell. Since the receptors in their physical characteristics differ from adenylate cyclase, the set of receptors located on the cell surface determines the specific picture of its sensitivity to external chemical signals. An individual cell may have three or more different inhibitory receptors and six or more different stimulatory receptors. Conversely, all cells appear to contain similar (possibly identical) G and AC components.

The molecular components of the hormone-sensitive adenylate cyclase provide checkpoints for changing the sensitivity of a given tissue to hormonal stimulation. Both P and G components are critical factors in the physiological regulation of hormone sensitivity, and changes in G proteins are considered the primary lesion occurring in the four diseases discussed below.

Regulation of sensitivity to hormones (see also Chapter 66). Repeated administration of any hormone or drug, as a rule, causes a gradual increase in resistance to their action. This phenomenon has different names: hyposensitization, refractoriness, tachyphylaxis or tolerance.

Hormones or mediators can cause the development of hyposensitization, which is receptor-specific, or "homologous". For example, the administration of β-adrenergic catecholamines causes specific myocardial refractoriness to repeated administration of these amines, but not to those drugs that do not act through β-adrenergic receptors. Receptor-specific desensitization involves at least two separate mechanisms. The first of them, rapidly developing (within a few minutes) and rapidly reversible upon removal of the injected hormone, functionally “uncouples” the receptors and the Gs protein and, consequently, reduces their ability to stimulate adenylate cyclase. The second process is associated with the actual decrease in the number of receptors on the cell membrane - a process called receptor downregulation. The process of receptor downregulation takes several hours to develop and is difficult to reverse.

Desensitization processes are part of normal regulation. The elimination of normal physiological stimuli can lead to an increase in the sensitivity of the target tissue to pharmacological stimulation, as occurs with the development of denervation-induced hypersensitivity. A potentially important clinical correlation of such an increase in the number of receptors may develop in patients with a sudden cessation of treatment with anaprilin, which is a β-adrenergic blocking agent. In such patients, transient signs of increased sympathetic tone (tachycardia, increased blood pressure, headaches, trembling, etc.) are often observed and symptoms of coronary insufficiency may develop. In the peripheral blood leukocytes of patients receiving anaprilin, an increased number of b-adrenergic receptors is found, and the number of these receptors slowly returns to normal values upon discontinuation of the drug. Although more numerous other leukocyte receptors do not mediate the cardiovascular symptoms and events that occur when anaprilin is discontinued, receptors in the myocardium and other tissues are likely to undergo the same changes.

The sensitivity of cells and tissues to hormones can also be regulated in a "heterologous" way, that is, when sensitivity to one hormone is regulated by another hormone acting through a different set of receptors. Regulation of the sensitivity of the cardiovascular system to b-adrenergic amines by hormones thyroid gland is the best-known clinical example of heterologous regulation. Thyroid hormones cause the accumulation of an excess amount of b-adrenergic receptors in the myocardium. This is an increase. The number of receptors partially explains the increased sensitivity of the heart of patients with hyperthyroidism to catecholamines. However, the fact that in experimental animals the increase in the number of β-adrenergic receptors caused by the administration of thyroid hormones is not enough to attribute an increase in the sensitivity of the heart to catecholamines to its account, suggests that the components of the response to hormones are also affected by thyroid hormones. , acting distal to the receptors, possibly including, but not limited to, Gs. Other examples of heterologous regulation include estrogen and progesterone's control of uterine sensitivity to the relaxing effects of β-adrenergic agonists and the increased reactivity of many tissues to adrenaline induced by glucocorticoids.

The second type of heterologous regulation is the inhibition of hormonal stimulation of adenylate cyclase by substances acting through Pu and Gi, as noted above. Acetylcholine, opiates, and a-adrenergic catecholamines act through distinct classes of inhibitory receptors (muscarinic, opiate, and a-adrenergic receptors) to desensitize adenylate cyclase in certain tissues to the stimulatory effects of other hormones. Although the clinical significance of this type of heterologous regulation has not been established, inhibition of cyclic AMP synthesis by morphine and other opiates could be responsible for some aspects of tolerance to this class of drugs. Similarly, the elimination of such oppression may play a role in the development of the syndrome following the cessation of opiate administration.

The nervous regulation of the work of the heart is carried out by sympathetic and parasympathetic impulses. The former increase the frequency, strength of contractions, blood pressure, and the latter have the opposite effect. Age-related changes in the tone of the autonomic nervous system are taken into account when prescribing treatment.

📌 Read this article

Features of the sympathetic nervous system

The sympathetic nervous system is designed to activate all body functions in a stressful situation. It provides a fight-or-flight response. Under the influence of irritation of the nerve fibers that enter it, the following changes occur:

  • weak bronchospasm;
  • narrowing of the arteries, arterioles, especially those located in the skin, intestines and kidneys;
  • contraction of the uterus, bladder sphincters, spleen capsule;
  • spasm of the rainbow muscle, pupil dilation;
  • decrease in motor activity and tone of the intestinal wall;
  • accelerated .

Strengthening of all cardiac functions - excitability, conductivity, contractility, automaticity, splitting of adipose tissue and the release of renin by the kidneys (increases pressure) are associated with irritation of beta-1 adrenergic receptors. And stimulation of beta-2 type leads to:

  • expansion of the bronchi;
  • relaxation of the muscular wall of arterioles in the liver and muscles;
  • breakdown of glycogen;
  • the release of insulin to carry glucose into cells;
  • energy generation;
  • decrease in uterine tone.

The sympathetic system does not always have a unidirectional effect on the organs, which is associated with the presence of several types of adrenergic receptors in them. Ultimately, the tolerance of physical and mental stress increases in the body, the work of the heart and skeletal muscles increases, and blood circulation is redistributed to nourish vital organs.

What is the difference between the parasympathetic system

This section of the autonomic nervous system is designed to relax the body, recover from stress, ensure digestion and energy storage. When the vagus nerve is activated:

  • increased blood flow to the stomach and intestines;
  • increased release of digestive enzymes and bile production;
  • the bronchi narrow (at rest, a lot of oxygen is not required);
  • the rhythm of contractions slows down, their strength decreases;
  • decreases the tone of the arteries and.

Influence of two systems on the heart

Despite the fact that sympathetic and parasympathetic stimulation have opposite effects on the cardiovascular system, this is not always so clear-cut. And the mechanisms of their mutual influence do not have a mathematical pattern, not all of them have been sufficiently studied, but it has been established:

  • the more the sympathetic tone rises, the stronger the suppressive effect of the parasympathetic department will be - the accentuated opposition;
  • when the desired result is achieved (for example, acceleration of the rhythm during exercise), the sympathetic and parasympathetic influence is inhibited - functional synergism (unidirectional action);
  • the higher the initial level of activation, the less the possibility of its increase during stimulation - the law of the initial level.

Watch the video about the effect on the heart of the sympathetic and parasympathetic systems:

Effect of age on autonomic tone

In newborns, the influence of the sympathetic department predominates against the background of a general immaturity of nervous regulation. Therefore, they are significantly accelerated. Then both parts vegetative system develop very quickly, reaching a maximum by adolescence. At this time, the highest concentration of nerve plexuses in the myocardium is noted, which explains the rapid change in pressure and contraction rate under external influences.

Up to 40 years, parasympathetic tone prevails, which affects the slowing of the pulse at rest and its rapid return to normal after exercise. And then they begin age-related changes- the number of adrenoreceptors is reduced while maintaining the parasympathetic ganglia. This leads to the following processes:

  • the excitability of muscle fibers worsens;
  • the processes of formation of impulses are violated;
  • increases the sensitivity of the vascular wall and myocardium to the action of stress hormones.

Under the influence of ischemia, the cells acquire an even greater response to sympathetic impulses and respond to even the slightest signals with spasm of the arteries and an acceleration of the pulse. This increases the electrical instability of the myocardium, which explains frequent occurrence at , and especially at .

It has been proven that disturbances in sympathetic innervation are many times greater than the destruction zone during acute disorder coronary circulation.

What happens when aroused

In the heart, there are mainly beta 1 adrenoreceptors, a little beta 2 and alpha type. At the same time, they are located on the surface of cardiomyocytes, which increases their availability for the main mediator (conductor) of sympathetic impulses - norepinephrine. Under the influence of activation of receptors, the following changes occur:

  • the excitability of the cells of the sinus node, the conduction system, muscle fibers increases, they even respond to subthreshold signals;
  • conduction of an electrical impulse is accelerated;
  • the amplitude of contractions increases;
  • the number of heartbeats per minute increases.

Parasympathetic cholinergic receptors of type M were also found on the outer membrane of the heart cells. Their excitation inhibits the activity of the sinus node, but at the same time increases the excitability of the atrial muscle fibers. This can explain the development of supraventricular extrasystole at night, when the tone of the vagus nerve is high.

The second depressive effect is the inhibition of the parasympathetic conduction system in the atrioventricular node, which delays the propagation of signals to the ventricles.

Thus, the parasympathetic nervous system:

  • reduces the excitability of the ventricles and increases it in the atria;
  • slows down the heart rate;
  • inhibits the formation and conduction of impulses;
  • suppresses the contractility of muscle fibers;
  • reduces myocardial oxygen demand;
  • prevents spasm of the walls of arteries and.

Sympathicotonia and vagotonia

Depending on the predominance of the tone of one of the sections of the autonomic nervous system, patients may have an initial increase in sympathetic effects on the heart - sympathicotonia and vagotonia with excessive parasympathetic activity. This is important when prescribing treatment for diseases, since the reaction to medications can be different.

For example, with initial sympathicotonia, patients can be identified:

  • the skin is dry and pale, the extremities are cold;
  • the pulse is accelerated, the increase in systolic and pulse pressure predominates;
  • sleep is disturbed;
  • psychologically stable, active, but there is high anxiety.

For such patients, it is necessary to use sedative drugs and adrenoblockers as the basis of drug therapy. With vagotonia, the skin is moist, there is a tendency to faint with a sharp change in body position, movements are slowed down, exercise tolerance is low, the difference between systolic and diastolic pressure is reduced.

For therapy, it is advisable to use calcium antagonists,.

Sympathetic nerve fibers and the mediator norepinephrine ensure the activity of the body under the action of stress factors. With stimulation of adrenoreceptors, pressure rises, the pulse accelerates, excitability and conduction of the myocardium increase.

The parasympathetic division and acetylcholine have an opposite effect on the heart, they are responsible for relaxation and energy accumulation. Normally, these processes successively replace each other, and in violation of the nervous regulation (sympathicotonia or vagotonia), the blood circulation parameters change.

Read also

There are heart hormones. They affect the work of the body - reinforcing, slowing down. It can be hormones of the adrenal glands, thyroid gland and others.

  • In itself, an unpleasant VSD, and panic attacks along with it can bring a lot of unpleasant moments. Symptoms - fainting, fear, panic and other manifestations. How to get rid of it? What is the treatment, and also what is the connection with nutrition?
  • For those who suspect that they have heart rhythm problems, it is useful to know the causes and symptoms of atrial fibrillation. Why does it arise and develop in men and women? What is the difference between paroxysmal and idiopathic atrial fibrillation?
  • The dromotropic effect means a violation of the change in the impulse of the heart. There are negative and positive. Medications for detection are selected strictly on an individual basis.
  • Autonomic dysfunction occurs under a number of factors. In children, adolescents, adults, the syndrome is most often diagnosed due to stress. Symptoms can be confused with other diseases. Treatment of autonomic nervous dysfunction is a complex of measures, including drugs.
  • Content

    Parts of the autonomic system are the sympathetic and parasympathetic nervous systems, the latter having a direct impact and being closely related to the work of the heart muscle, the frequency of myocardial contraction. It is localized partially in the brain and spinal cord. The parasympathetic system provides relaxation and recovery of the body after physical, emotional stress, but cannot exist separately from the sympathetic department.

    What is the parasympathetic nervous system

    The department is responsible for the functionality of the organism without its participation. For example, parasympathetic fibers provide respiratory function, regulate heartbeat, dilate blood vessels, control natural process digestion and protective functions, provide other important mechanisms. The parasympathetic system is necessary for a person to relax the body after physical activity. With its participation, muscle tone decreases, the pulse returns to normal, the pupil narrows and vascular walls. This happens without human intervention - arbitrarily, at the level of reflexes

    The main centers of this autonomous structure are the brain and spinal cord, where nerve fibers are concentrated, providing the fastest possible transmission of impulses for the operation of internal organs and systems. With their help, you can control blood pressure, vascular permeability, cardiac activity, internal secretion of individual glands. Each nerve impulse is responsible for a certain part of the body, which, when excited, begins to react.

    It all depends on the localization of the characteristic plexuses: if the nerve fibers are in the pelvic area, they are responsible for physical activity, and in the digestive system organs - for the secretion of gastric juice, intestinal motility. The structure of the autonomic nervous system has the following constructive sections with unique functions for the whole organism. It:

    • pituitary;
    • hypothalamus;
    • nervus vagus;
    • epiphysis

    This is how the main elements of the parasympathetic centers are designated, and the following are considered additional structures:

    • nerve nuclei of the occipital zone;
    • sacral nuclei;
    • cardiac plexuses to provide myocardial shocks;
    • hypogastric plexus;
    • lumbar, celiac and thoracic nerve plexuses.

    Sympathetic and parasympathetic nervous system

    Comparing the two departments, the main difference is obvious. The sympathetic department is responsible for activity, reacts in moments of stress, emotional arousal. As for the parasympathetic nervous system, it "connects" in the stage of physical and emotional relaxation. Another difference is the mediators that carry out the transition of nerve impulses in synapses: in sympathetic nerve endings it is norepinephrine, in parasympathetic nerve endings it is acetylcholine.

    Features of interaction between departments

    The parasympathetic division of the autonomic nervous system is responsible for the smooth operation of the cardiovascular, genitourinary and digestive systems, while parasympathetic innervation of the liver, thyroid gland, kidneys, and pancreas takes place. The functions are different, but the impact on the organic resource is complex. If the sympathetic department provides excitation of the internal organs, then the parasympathetic one helps to restore general state organism. If there is an imbalance of the two systems, the patient needs treatment.

    Where are the centers of the parasympathetic nervous system located?

    The sympathetic nervous system is structurally represented by the sympathetic trunk in two rows of nodes on both sides of the spine. Externally, the structure is represented by a chain of nerve lumps. If we touch on the element of so-called relaxation, the parasympathetic part of the autonomic nervous system is localized in the spinal cord and brain. So, from the central sections of the brain, the impulses that arise in the nuclei go as part of the cranial nerves, from the sacral sections - as part of the pelvic splanchnic nerves, reach the organs of the small pelvis.

    Functions of the parasympathetic nervous system

    The parasympathetic nerves are responsible for natural recovery body, normal myocardial contraction, muscle tone and productive relaxation of smooth muscles. Parasympathetic fibers differ in local action, but in the end they act together - plexuses. With a local lesion of one of the centers, the autonomic nervous system as a whole suffers. The effect on the body is complex, and doctors distinguish the following useful functions:

    • relaxation oculomotor nerve, constriction of the pupil;
    • normalization of blood circulation, systemic blood flow;
    • restoration of habitual breathing, narrowing of the bronchi;
    • lowering blood pressure;
    • control of an important indicator of blood glucose;
    • reduction in heart rate;
    • slowing down the passage of nerve impulses;
    • decline eye pressure;
    • regulation of the glands of the digestive system.

    In addition, the parasympathetic system helps the vessels of the brain and genital organs to expand, and the smooth muscles to tone up. With its help, a natural cleansing of the body occurs due to such phenomena as sneezing, coughing, vomiting, going to the toilet. In addition, if symptoms begin to appear arterial hypertension, it is important to understand that the above-described nervous system is responsible for cardiac activity. If one of the structures - sympathetic or parasympathetic - fails, measures must be taken, since they are closely related.

    Diseases

    Before using any medical preparations, to do research, it is important to correctly diagnose diseases associated with impaired functioning of the parasympathetic structure of the brain and spinal cord. The health problem manifests itself spontaneously, it can hit internal organs to affect habitual reflexes. The following violations of the body of any age may be the basis:

    1. Cyclic paralysis. The disease is provoked by cyclic spasms, severe damage to the oculomotor nerve. The disease occurs in patients of different ages, accompanied by degeneration of the nerves.
    2. Syndrome of the oculomotor nerve. In such a difficult situation, the pupil can expand without exposure to a stream of light, which is preceded by damage to the afferent section of the pupillary reflex arc.
    3. Block nerve syndrome. A characteristic ailment is manifested in a patient by a slight strabismus, imperceptible to a simple man in the street, while eyeball directed inward or upward.
    4. Injured abducens nerves. In the pathological process, they are simultaneously combined in one clinical picture strabismus, double vision, severe Fauville's syndrome. Pathology affects not only the eyes, but also the facial nerves.
    5. Trigeminal nerve syndrome. Among the main causes of pathology, doctors distinguish an increased activity of pathogenic infections, a violation of systemic blood flow, damage to the cortical-nuclear pathways, malignant tumors, traumatic brain injury.
    6. Syndrome facial nerve. There is an obvious distortion of the face, when a person arbitrarily has to smile, while experiencing pain. More often it is a complication of the disease.