Humoral regulation of vascular tone physiology. Neurohumoral regulation of vascular tone

The cells' needs for oxygen and nutrients are ensured by maintaining a constant blood pressure level and redistributing blood between working and non-working organs. The constancy of blood pressure is maintained due to the continuous maintenance of correspondence between the value of cardiac output and the value of the total peripheral resistance of the vascular system, which depends on vascular tone.

Vascular smooth muscles, even after eliminating all external nervous and humoral influences, have a basal tone. Its occurrence is due to the fact that in some areas of smooth muscle there are foci of automaticity that generate rhythmic impulses that spread to other muscle cells, creating basal tone. In addition, vascular smooth muscles are under constant sympathetic influence, which is formed in the vasomotor center and maintains a certain degree of their contraction.

Nervous regulation of the lumen of blood vessels is carried out mainly by SS, which exerts its influence through α- and β-adrenergic receptors. Excitation of α-adrenergic receptors leads to vasoconstriction, β-adrenergic receptors - to dilation. SS narrows the arteries of the skin and mucous membranes, abdominal cavity, limbs, dilates the vessels of skeletal working muscles. PS causes dilation of the vessels of the submandibular salivary gland, tongue, penis.

The vasomotor center is located in the medulla oblongata at the bottom of the IV ventricle and consists of 2 sections: pressor and depressor. The pressor region exerts its influence through the sympathetic nuclei of the spinal cord. The tone of the vasomotor center depends on afferent signals coming from the receptors of the reflexogenic zones of the vascular bed, as well as on humoral factors acting directly on the nerve center. Vascular reflexes can be divided into two groups.

Own vascular reflexes are caused by signals from vascular receptors. An increase in blood pressure in the aortic arch and carotid sinus irritates the baroreceptors of these zones. Impulses along the aortic and sinocarotid nerves go to the medulla oblongata and reduce the tone of the X nuclei. As a result, the work of the heart is inhibited, the vessels dilate and blood pressure decreases. A decrease in blood pressure due, for example, to a decrease in blood volume during blood loss, weakening of the heart, or during the redistribution of blood and its outflow into excessively dilated vessels of a large organ, leads to less intense irritation of baroreceptors. The influence of the aortic and sinocarotid nerves on the neurons of the X and vasoconstrictor center is weakened. As a result, the work of the heart increases, the vessels narrow and blood pressure normalizes. Stretch receptors are located in both atria and at the mouth of the superior and inferior vena cava. When the right atrium is overflowing with blood, impulses from these receptors travel through sensory fibers X to the medulla oblongata, reducing the tone of the nuclei X, increasing SS tone. There is an increase in cardiac activity and constriction of blood vessels.

Reflex regulation of blood pressure is also carried out using chemoreceptors. They are especially numerous in the aortic arch and carotid sinus. They are sensitive to a lack of O 2 and are irritated by CO, CO 2, cyanide, and nicotine. Impulses from these receptors enter the vasomotor center, increasing the tone of the pressor region, which leads to vasoconstriction and increased blood pressure. At the same time, the respiratory center is excited.

Associated vascular reflexes occur in other systems and organs and are manifested primarily by an increase in blood pressure. For example, when painful stimulation occurs, blood vessels reflexively constrict, especially in the abdominal cavity. Skin irritation from cold causes constriction of cutaneous arterioles.

Humoral regulation of vascular tone.

Vasoconstrictor substances.

1. Catecholamines (adrenaline and norepinephrine) are constantly secreted in small quantities by the adrenal medulla and circulate in the blood. NA is also

mediator of the SS vasomotor nerves. Of the catecholamines secreted by the adrenal glands, 80% are A and 20% are NA. The reactions of blood vessels to them may be different.

NA causes a weak response of β-adrenergic receptors in vascular smooth muscle, acting predominantly on α-adrenergic receptors and causing vasoconstriction. A acts on both α- and β-adrenergic receptors. There are both adrenergic receptors in the vessels, but the quantitative ratio in different parts of the vascular system is different. If α-adrenergic receptors predominate, then A causes their narrowing, β-adrenergic receptors - expansion. Under physiological conditions, with a normal, sufficiently low level of A in the blood, it has a dilating effect on the muscular arteries, since the effect of β-adrenergic receptors predominates. With a high level of A in the blood, the vessels narrow as a result of the predominance of the effect of α-adrenergic receptors.

2. Vasopressin (ADH) in medium and high doses has a vasoconstrictor effect, most pronounced at the level of arterioles. Vasopressin also plays a special role in the regulation of intravascular fluid volume. With an increase in blood volume, impulses from atrial receptors increase, resulting in 10-20 minutes. the release of vasopressin is reduced, which leads to an increase in fluid excretion by the kidneys. As blood pressure falls, ADH release increases and fluid secretion decreases.

3. Serotonin is formed in the intestinal mucosa, brain, and during the breakdown of platelets. The physiological significance of serotonin is that it constricts blood vessels, preventing bleeding. In the 2nd phase of blood coagulation, which develops after the formation of a blood clot, serotonin dilates blood vessels.

4. Renin is an enzyme that is produced by the kidneys in response to a decrease in blood pressure. It breaks down plasma α 2 globulin - angiotensinogen to angiotensin I, which is converted into angiotensin II.

Angiotensin II has a strong vasoconstrictor effect on arteries and less strong on veins, and also stimulates central and peripheral SS structures. As a result, peripheral resistance increases. The effect of the renin-angiotensin system reaches its maximum after 20 minutes. and continues for a long time. This system plays an important role in normalizing blood circulation with a pathological decrease in blood pressure and/or blood volume.

Angiotensin is also the main stimulator of aldosterone production in the adrenal cortex. Aldosterone promotes sodium reabsorption in the renal tubules and collecting ducts, increasing water retention in the kidneys. At the same time, aldosterone increases the sensitivity of vascular smooth muscle to vasoconstrictor agents, thereby increasing the pressor effect of angiotensin II. Excessive production of aldosterone leads to hypertension, decreased production leads to hypotension.

Given the close relationship between renin, angiotensin and aldosterone, their effects are combined under the name renin-angiotensin-aldosterone system.

Vasodilators.

1. Prostaglandins are formed in many organs and tissues from polyunsaturated fatty acids (arachidonic, linoleic), which are part of the phospholipid fractions of biological membranes. PGA 1 and PGA 2 cause dilation of the arteries, especially the celiac region. Medullin (PGA 2), isolated from the medulla of the kidney, reduces blood pressure, increases renal blood flow and the release of H 2 O, Na +, K + by the kidneys.

2. Kallikrein-kinin system. Kallikrein is an enzyme found in tissues and plasma in an inactive form. Once activated, it breaks down plasma α2 globulin to kallidin, which is converted to bradykinin. Callidin and bradykinin have a pronounced vasodilatory effect and increase capillary permeability. The dilation of blood vessels in the glands of the gastrointestinal tract with an increase in their activity, and an increase in blood flow in the vessels of the skin during sweating are provided mainly by kinins.

3. Histamine is formed in the gastrointestinal mucosa, in the skin during irritation, in skeletal muscles during work and in other organs. It causes local dilation of arterioles and venules and increases capillary permeability.

4. The degree of contraction of vascular muscles is directly influenced by some substances necessary for cellular metabolism (for example O 2), or produced during the metabolic process. These substances provide metabolic autoregulation of peripheral circulation, which adapts local blood flow to the functional needs of the organ. Thus, a decrease in the partial pressure of O 2 causes local dilation of blood vessels. Vasodilation also occurs with a local increase in CO 2 or H + voltage. ATP, ADP, AMP, adenosine, ACh, and lactic acid have a vasodilating effect.

In this part we are talking about the nervous and humoral regulation of vascular tone: about the efferent innervation of blood vessels, about a brief description of the vasomotor centers, about the reflex regulation of vascular tone, about the humoral regulation of vascular tone.

Nervous and humoral regulation of vascular tone.

The blood supply to the organs depends on the size of the lumen of the vessels, their tone and the amount of blood ejected into them by the heart. Therefore, when considering the regulation of vascular function, we should first of all talk about the mechanisms of maintaining vascular tone and the interaction of the heart and blood vessels.

Efferent innervation of blood vessels.

Vascular lumen is mainly regulated by the sympathetic nervous system. Its nerves, independently or as part of mixed motor nerves, approach all arteries and arterioles and exert a vasoconstrictor effect. A clear demonstration of this influence is the experiments of Claude Bernard, carried out on the vessels of the rabbit ear. In these experiments, the sympathetic nerve was cut on one side of the rabbit's neck, after which redness of the ear of the operated side and a slight increase in its temperature were observed due to vasodilation and increased blood supply to the ear. Irritation of the peripheral end of the cut sympathetic nerve caused vasoconstriction and blanching of the ear.

The sympathetic nerves, which innervate most of the vessels of the abdominal cavity, approach them as part of the splanchnic nerve. Sympathetic fibers travel to the vessels of the extremities together with motor nerves.

Under the influence of the sympathetic nervous system, the vascular muscles are in a state of contraction - tonic tension.

Under natural conditions of the body's life, changes in the lumen of most vessels (their dilation and expansion) occur due to changes in the number of impulses traveling along the sympathetic nerves. The frequency of these pulses is low - approximately one pulse per second. Under the influence of reflex effects, their number can be increased or decreased. With an increase in the number of impulses, the tone of the vessels increases - they narrow. If the number of impulses decreases, the vessels dilate.

The parasympathetic nervous system has a vasodilating effect only on the vessels of certain organs. In particular, it dilates the blood vessels of the tongue, salivary glands and genitals. Only these three organs have double innervation: sympathetic (vasoconstrictor) and parasympathetic (vasodilator).

Brief characteristics of vasomotor centers.

The neurons of the sympathetic nervous system, through the processes of which impulses travel to the vessels, are located in the lateral horns of the gray matter of the spinal cord. The level of activity of these neurons depends on the influences of the overlying parts of the central nervous system.

In 1871, F.V. Ovsyannikov showed that in the medulla oblongata there are neurons, under the influence of which vasoconstriction occurs. This center is called the vasomotor center. Its neurons are concentrated in the medulla oblongata at the bottom of the fourth ventricle near the nucleus of the vagus nerve.

In the vasomotor center, two sections are distinguished: pressor, or vasoconstrictor, and depressor, or vasodilator. When the neurons of the pressor center are irritated, vasoconstriction occurs and blood pressure increases, and when the depressor center is irritated, vasodilation occurs and blood pressure decreases. The neurons of the depressor center at the moment of their excitation cause a decrease in the tone of the pressor center, as a result of which the number of tonic impulses going to the vessels decreases and their dilation occurs.

Impulses from the vasoconstrictor center of the brain arrive at the lateral horns of the gray matter of the spinal cord, where the neurons of the sympathetic nervous system are located, forming the vasoconstrictor center of the spinal cord. From it, along the fibers of the sympathetic nervous system, impulses go to the muscles of the blood vessels and cause their contraction, as a result of which vasoconstriction occurs.

Reflex regulation of vascular tone.

There are intrinsic cardiovascular reflexes and associated ones.

Conjugate cardiovascular reflexes are divided into two groups: exteroceptive (arising from irritation of receptors lying on the surface of the body) and interoreceptive (arising from irritation of receptors in internal organs).

Any effect on the body that comes from exteroceptors primarily increases the tone of the vasomotor center and causes a pressor reaction. Thus, with mechanical or painful irritation of the skin, strong irritation of the visual and other receptors, a reflex vasoconstriction occurs.

Vascular reactions are associated with the redistribution of blood in the body and the blood supply to working organs.

Particularly important in the redistribution of blood in the body are the reactions that occur when interoreceptors and receptors from working muscles are irritated. Providing working muscles with oxygen and nutrients occurs due to vasodilation and increased blood supply to working muscles. Vasodilation occurs when chemoreceptors are irritated by metabolic products - ATP, lactic, carbonic and other acids, which cause a decrease in tone and dilation of blood vessels. More blood enters the dilated vessels, thereby improving the nutrition of working muscles. But at the same time, redistribution of blood occurs reflexively. Under the influence of efferent impulses from the vasomotor center, vasoconstriction of non-functioning organs occurs. The dilated vessels of working organs turn out to be insensitive to these vasoconstrictor impulses.

Humoral regulation of vascular tone.

Chemicals that affect the lumen of blood vessels are divided into vasoconstrictors and vasodilators.

Adrenaline and norepinephrine have the most powerful vasoconstrictor effects. They cause narrowing of the arteries and arterioles of the skin, lungs and abdominal organs. At the same time, they cause dilation of blood vessels in the heart and brain.

Adrenaline is a biologically very active drug and acts in very small concentrations. 0.0002 mg of adrenaline per 1 kg of body weight is enough to cause vasoconstriction and an increase in blood pressure. The vasoconstrictor effect of adrenaline occurs in different ways. It acts directly on the vascular wall and reduces the membrane potential of its muscle fibers, increasing excitability and creating conditions for the rapid occurrence of excitation. Adrenaline affects the hypothalamus and leads to an increase in the flow of vasoconstrictor impulses and an increase in the amount of vasopressin released.

Renin produced in the kidneys has an indirect effect on changes in the lumen of blood vessels and maintaining a constant blood pressure. Its formation increases as the amount of sodium in the blood decreases and blood pressure decreases. Interacting with the plasma protein hypertensinogen, it forms the biologically active substance hypertensin, which causes vasoconstriction and an increase in blood pressure.

Vasoconstrictor factors include serotonin, which, by narrowing the damaged vessel, helps reduce bleeding.

Acetylcholine, antihypertensinogen, medulin, bradykinin, prostaglandins, histamine, etc. have a vasodilating effect.

Acetylcholine causes dilation of small arteries and a decrease in blood pressure. Its effect is short-lived, as it is quickly destroyed in the blood.

Antihypertensinogen is constantly in the blood along with hypertensinogen, balancing its effect. Fluctuations in its amount in the blood are aimed at maintaining constant blood pressure.

Medulin is formed in the kidneys, causing vasodilation.

Bradykinin is formed in the tissues of the pancreas and submandibular glands, in the lungs, skin, etc. It reduces the tone of the smooth muscles of arterioles, helping to lower blood pressure.

Histamine is formed in the process of metabolism in skeletal muscles, in the skin, in the walls of the stomach and intestines, etc. Under the influence of histamine, arterioles dilate and the blood supply to the capillaries increases, and therefore a large amount of blood is retained in them. Therefore, blood flow to the heart is reduced, which leads to a drop in blood pressure in the arteries.

The degree of tension of the smooth muscles of the vascular wall is called tone. When it increases, resistance to blood flow increases, blood pressure increases; with low tone, the lumen of the arteries becomes larger and the pressure drops. This process is influenced by nervous mechanisms - sympathetic and parasympathetic innervation, the vasomotor center of the brain, as well as a significant amount of hormones and biologically active compounds.

Violation of normal tone leads to hypertension or hypotension.

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Why is vascular tone needed?

With the help of vascular tone, the body regulates one of the main parameters - blood pressure. Its normal level ensures adequate nutrition of internal organs, including the myocardium and brain. How the vascular wall reacts to changes in the parameters of the internal and external environment determines a person’s well-being during changes in atmospheric pressure, increased physical activity, and the influence of stress factors.

In healthy people, especially with good training of the cardiovascular system, rapid expansion and contraction of the arteries occurs in response to stress, and then the vascular tone also quickly returns to normal. At the same time, all organs and tissues receive a sufficient amount of blood, which means oxygen and nutrients, metabolic processes are activated, and additional stress is easily tolerated.

In cases of illness, in elderly people, a slow reaction is observed in response to an irritant; it is not enough to cover the increased nutritional needs; a paradoxical narrowing of blood vessels may also occur instead of their dilation, and vice versa.

The initial vascular tone is maintained by the work of smooth muscles. At the same time, the coronary arteries, vessels of skeletal muscles and kidneys have high tone, and the skin and mucous membranes are fed by arteries with low tone. When exposed to an intense stimulus, the high tone decreases and the low tone increases.

Regulatory mechanisms

Control and maintenance of the necessary parameters of the lumen of the vessel is carried out by three mechanisms - local (autonomous regulation), nervous and humoral (through blood, tissue fluid).

Nervous

The tone of the vascular wall is directly influenced by impulses that come from the vasomotor center of the brain. It transmits a signal about the narrowing of the lumen of the arteries through sympathetic fibers, and about expansion through parasympathetic signals.

The second level (reflex) are the structures of the carotid sinus, aorta and pulmonary artery. They contain receptors that perceive blood pressure, its alkaline reaction, oxygen and carbon dioxide content. Through nerve fibers, information comes to the centers of the spinal cord. Due to this control link, blood flow is redistributed under stress conditions - vital organs receive an advantage in nutrition, even to the detriment of others.

More subtle regulation is carried out by the hypothalamus. It changes the activity of some parts of the autonomic fibers, inhibiting signals from others. This occurs due to the following mechanisms:

  • Sympathetic nerves reduce the diameter of blood vessels in the skin, mucous membranes and digestive system, dilate coronary and cerebral arteries, pulmonary and skeletal muscles.
  • Parasympathetic dilates the blood vessels of the tongue, glands of the oral cavity, choroid of the brain and genitals.
  • Axon reflexes have a local vasodilator effect. An example is the redness of the skin when its receptors are irritated.

Humoral

At the local level, blood electrolytes regulate vascular tone - calcium and sodium constrict blood vessels and increase blood pressure, while potassium and magnesium have the opposite effect. Autonomous regulators also include:

  • metabolic products (carbon dioxide, organic acids, hydrogen ions) accelerate the transmission of impulses to the brain, constrict blood vessels;
  • histamine, bradykinin and prostaglandins reduce tone;
  • serotonin, enzymes of the endothelium (inner lining) have a vasoconstrictor effect.

Systemic regulation of vascular tone is carried out by hormones secreted by endocrine glands:

  • adrenaline and norepinephrine constrict all arteries except the brain, kidney and skeletal muscles;
  • vasopressin reduces the lumen of veins, and angiotensin 2 arteries and arterioles;
  • adrenal corticosteroids and thyroxine gradually increase vascular tone due to sympathetic impulses.

Local

This is the reaction of the vessel to two main parameters - pressure and blood flow rate. At high pressure, smooth muscle fibers are stretched, which causes their reflex contraction and increased resistance. When the pressure in the arteries decreases, the wall relaxes and does not interfere with the flow of blood. These processes do not require the participation of the brain.

Violation of local regulation can occur with a lack of oxygen, blood loss, dehydration, and low physical activity.


Vessel blockage

What affects vascular tone

Any change in the internal or external environment affects the activity of the cardiovascular system. The most common causes of significant fluctuations in vascular tone are:

  • decrease or increase in atmospheric pressure, climate change;
  • genetic characteristics of the nervous system reaction;
  • stressful situations;
  • infectious diseases;
  • poisoning with chemical compounds, medications, alcohol or nicotine;
  • skull injuries;
  • diabetes;
  • thyroid diseases;
  • imbalance of sex hormones;
  • obesity;
  • low physical activity.

What will violations tell you about (decrease, increase)

Fluctuations in vascular tone are normal reactions to changes in the internal and external environment. Painful conditions occur only with a persistent increase or decrease.

Low tone - hypotension

There is a decrease in blood pressure below 100/60 mm Hg. Art. In this case, the general weak tone cannot be compensated by a local increase in the resistance of arterioles or capillaries.

Typical clinical manifestations are:

  • general weakness,
  • fast fatiguability,
  • headache,
  • dizziness,
  • fainting states,
  • heartache.

The causes of persistent hypotension may be congenital asthenia, low activity of the adrenal glands, thyroid gland, and pituitary gland. A decrease in pressure is observed with exhaustion, prolonged infection, and intoxication. The most severe conditions occur with shock or that accompany injuries, burns, anaphylactic reactions, and acute heart failure.

Watch the video about hypotension, its causes and treatment:

Hypertension

The mechanism of high arterial wall resistance in old age is most often associated with sclerotic changes and loss of vascular elasticity. At a younger age, vascular spasm plays a major role. It occurs when regulation on the part of the central nervous system or humoral link is disturbed. Most often there are changes in the activity of the vasomotor center.

Under the influence of long-term stress factors, the brain is overstrained, a persistent zone of excitation appears, which sends a constant stream of vasoconstrictor impulses to the arteries. The vascular response to irritation increases and sometimes becomes distorted.

A secondary increase in vascular tone occurs in the following diseases:

  • glomerulo- and pyelonephritis,
  • compression of kidney vessels,
  • disruption of the endocrine glands,
  • polio,
  • tumors and hemorrhages in the brain.

How to increase or decrease vascular tone

To normalize vascular tone, the following recommendations must be followed:

  • exercise regularly, cardio exercises are especially useful - walking, running, swimming;
  • have enough time to sleep;
  • carry out contrasting water procedures;
  • adhere to a diet and a healthy diet.

If there are diseases in which vascular tone is impaired, they must be treated by a specialist; self-medication in such cases can lead to fatal consequences.

Vascular tone reflects the state of regulatory mechanisms of the nervous system and endocrine organs. Its level is affected by all changes in the internal and external environment. In a healthy person, increases and decreases occur within physiological limits. The speed of return to initial parameters shows the level of fitness of the cardiovascular system.

In pathological conditions, the tone is increased (hypertension) or decreased (hypotension). Normalization of vascular resistance is carried out in the form of therapy for the underlying disease.

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Mexidol is used for cerebral vessels to improve blood circulation, relieve the negative manifestations of VSD and other things. Initially, injections are prescribed, then they switch to tablets. The medicine will help with spasms and for the heart. Does it narrow or dilate blood vessels?

  • If necessary, vascular rheoencephalography is performed to study the tone. Indications may include suspicions of atherosclerosis, hypo- and hypertension, dystonia and others. An REG can be performed with functional tests for a detailed examination of the blood supply to the brain.
  • Fainting occurs with vascular dystonia in severe cases. With VSD, you can prevent them by knowing simple rules of behavior. It is also important to understand how to provide assistance for fainting from vegetative-vascular dystonia.
  • Vascular vasospasm occurs due to mechanical problems or blockage of the bloodstream. It can be cerebral, peripheral, functional, or occur in the arteries of the brain or limbs. Symptoms in children and adults are pain. Treatment of vasospasm is individualized.
  • Coronary circulation plays an important function. Its features, pattern of movement in a small circle, blood vessels, physiology and regulation are studied by cardiologists if problems are suspected.


  • Arteries and arterioles are constantly in a state of narrowing, largely determined by the tonic activity of the vasomotor center. The tone of the vasomotor center depends on afferent signals coming from peripheral receptors located in some vascular areas and on the surface of the body, as well as on the influence of humoral stimuli acting directly on the nerve center.

    According to the classification of V.N. Chernigovsky, reflex changes in arterial tone - vascular reflexes - can be divided into two groups: intrinsic and associated reflexes.

    Own vascular reflexes are caused by signals from the receptors of the vessels themselves. Of particular importance to physiologists are the receptors concentrated in the aortic arch and in the area where the carotid artery branches into internal and external. These areas of the vascular system are called vascular reflexogenic zones.

    The receptors located in the aortic arch are the ends of centripetal fibers passing through the aortic nerve. Electrical stimulation of the central end of the nerve causes a drop in blood pressure due to a reflex increase in the tone of the vagus nerve nuclei and a reflex decrease in the tone of the vasoconstrictor center. As a result, cardiac activity is inhibited, and the vessels of the internal organs dilate.

    Receptors of vascular reflexogenic zones are excited when blood pressure in the vessels increases, which is why they are called pressoreceptors, or baroreceptors.

    Vascular reflexes can be caused by irritating the receptors not only of the aortic arch or carotid sinus, but also of the vessels of some other areas of the body. Thus, with an increase in pressure in the vessels of the lung, intestines, and spleen, reflex changes in blood pressure are observed in other vascular areas. Reflex regulation of blood pressure is carried out using not only mechanoreceptors, but also chemoreceptors, sensitive to changes in the chemical composition of the blood. Such chemoreceptors are concentrated in the aortic and carotid glomus.

    Conjugate vascular reflexes. These reflexes that occur in other systems and organs are manifested primarily by an increase in blood pressure. They can be caused, for example, by irritation of the body surface. Thus, during painful stimulation, blood vessels reflexively narrow, especially in the abdominal organs, and blood pressure rises.

    The vascular reaction to a previously indifferent stimulus is carried out in a conditioned reflex way, i.e., with the participation of the cerebral cortex. In this case, a person often experiences a corresponding sensation (cold, warm or pain), although there was no skin irritation.

    Nervous regulation of vascular tone is carried out by the autonomic nervous system, which has a vasoconstrictor and vasodilator effect.

    Sympathetic nerves are vasoconstrictors (constrict blood vessels) for the vessels of the skin, mucous membranes, gastrointestinal tract and vasodilators (dilate blood vessels) for the vessels of the brain, lungs, heart and working muscles. The parasympathetic part of the nervous system has a dilating effect on blood vessels.

    Humoral regulation is carried out by substances of systemic and local action. Systemic substances include calcium, potassium, sodium ions, and hormones. Calcium ions cause vasoconstriction, while potassium ions have a dilating effect.

    The effect of hormones on vascular tone:

    1. vasopressin - increases the tone of smooth muscle cells of arterioles, causing vasoconstriction;

    2. adrenaline has both a constricting and dilating effect, acting on alpha1-adrenergic receptors and beta1-adrenergic receptors, therefore, at low concentrations of adrenaline, dilation of blood vessels occurs, and at high concentrations, narrowing occurs;

    3. thyroxine - stimulates energy processes and causes constriction of blood vessels;

    4. renin - produced by cells of the juxtaglomerular apparatus and enters the bloodstream, influencing the protein angiotensinogen, which turns into angiotensin II, causing vasoconstriction.

    Metabolites (carbon dioxide, pyruvic acid, lactic acid, hydrogen ions) affect the chemoreceptors of the cardiovascular system, leading to a reflex narrowing of the lumen of blood vessels.

    Substances with local effects include:

    1. mediators of the sympathetic nervous system - vasoconstrictor, parasympathetic (acetylcholine) - dilating;

    2. biologically active substances - histamine dilates blood vessels, and serotonin constricts;

    3. kinins - bradykinin, kalidin - have an expanding effect;

    4. prostaglandins A1, A2, E1 dilate blood vessels, and F2b constricts.

    The heart is under constant action nervous system and humoral factors. The body is in different conditions of existence. The result of the work of the heart is the pumping of blood into the systemic and pulmonary circulation.

    It is estimated by minute blood volume. In a normal state, in 1 minute - 5 liters of blood are pushed out by both ventricles. This way we can evaluate the work of the heart.

    Systolic blood volume and heart rate - minute volume of blood.

    For comparison between different people - introduced cardiac index- what is the amount of blood per minute per 1 square meter of body.

    In order to change the volume value, you need to change these indicators, this happens due to the mechanisms of heart regulation.

    Minute blood volume (MBV) = 5 l/min

    Cardiac index=IOC/Sm2=2.8-3.6 l/min/m2

    IOC=systolic volume*frequency/min

    Mechanisms of cardiac regulation

    1. Intracardiac (intracardial)
    2. Extracardiac (Extracardiac)

    To intracardiac mechanisms include the presence of tight junctions between the cells of the working myocardium, the conduction system of the heart coordinates the individual work of the chambers, intracardiac nerve elements, hydrodynamic interaction between the individual chambers.

    Extracardiac - nervous and humoral mechanism, which change the work of the heart and adapt the work of the heart to the needs of the body.

    Nervous regulation of the heart is carried out by the autonomic nervous system. The heart receives innervation from parasympathetic(wandering) and sympathetic(lateral horns of the spinal cord T1-T5) nerves.

    Ganglia of the parasympathetic system lie inside the heart and there the preganglionic fibers switch to postganglionic. Preganglionic nuclei - medulla oblongata.

    Sympathetic- are interrupted in the stellate ganglion, where the postganglionic nerves that go to the heart will already be located.

    Right vagus nerve- innervates the sinoatrial node, the right atrium,

    Left vagus nerve to the atrioventricular node and right atrium

    Right sympathetic nerve- to the sinus node, right atrium and ventricle

    Left sympathetic nerve- to the atrioventricular nodes and to the left half of the heart.

    In the ganglia, acetylcholine acts on N-cholinergic receptors

    Sympathetic secrete norepinephrine, which acts on adrenergic receptors (B1)

    Parasympathetic- acetylcholine at M-cholino receptors (muscarino)

    Effect on heart function.

    1. Chronotropic effect (on heart rate)
    2. Inotropic (for the strength of heart contractions)
    3. Batmotropic effect (on excitability)
    4. Dromotropic (for conductivity)

    1845 - Weber brothers - discovered the influence of the vagus nerve. They cut the nerve in my neck. When the right vagus nerve was irritated, the frequency of contractions decreased, and could even stop - negative chronotropic effect(suppression of sinus node automation). If the left vagus nerve was irritated, conduction deteriorated. The atrioventricular nerve is responsible for the delay of excitation.

    Vagus nerves reduce myocardial excitability and reduce contraction frequency.

    Under the influence of the vagus nerve, the diastolic depolarization of p-cells, pacemakers, slows down. Potassium output increases. Although the vagus nerve causes cardiac arrest, it cannot be stopped completely. There is a resumption of heart contraction - escaping from the influence of the vagus nerve and the resumption of heart function due to the fact that the automation from the sinus node passes to the atrioventricular node, which returns the heart to work at a frequency 2 times less frequent.

    Sympathetic influences- studied by the Zion brothers - 1867. When irritating the sympathetic nerves, the Zions discovered that the sympathetic nerves give positive chronotropic effect. Pavlov studied further. In 1887 he published his work on the influence of nerves on the functioning of the heart. In his research, he discovered that individual branches, without changing the frequency, increase the strength of contractions - positive inotropic effect. Then the bamotropic and dromotropic effects were discovered.

    Positive effects on heart function occurs due to the influence of norepinephrine on beta 1 adrenoceptors, which activate adenylate cyclase, promote the formation of cyclic AMP, and increase the ionic permeability of the membrane. Diastolic depolarization occurs at a faster rate and this causes a more rapid rhythm. Sympathetic nerves increase the breakdown of glycogen and ATP, thereby providing the myocardium with energy resources, and the excitability of the heart increases. The minimum duration of an action potential in the sinus node is set to 120 ms, i.e. theoretically, the heart could give us a number of contractions - 400 per minute, but the atrioventricular node is not capable of conducting more than 220. The ventricles contract maximally at a frequency of 200-220. The role of mediators in the transmission of excitation to the hearts was established by Otto Lewy in 1921. He used 2 isolated frog hearts, and these hearts were fed from the 1st cannula. In one heart, nerve conductors were preserved. When one heart was irritated, he observed what happened in the other. When the vagus nerve is irritated, acetylcholine is released - through the fluid it affects the work of the other heart.

    The release of norepinephrine increases the work of the heart. The discovery of this mediator excitation brought Levy the Nobel Prize.

    The nerves of the heart are in a state of constant excitement - tone. At rest, the tone of the vagus nerve is especially pronounced. When the vagus nerve is cut, the heart rate increases by 2 times. The vagus nerves constantly inhibit the automation of the sinus node. Normal frequency is 60-100 contractions. Switching off the vagus nerves (transection, cholinergic receptor blockers (atropine)) causes the heart to work faster. The tone of the vagus nerves is determined by the tone of its nuclei. Excitation of the nuclei is maintained reflexively due to impulses that come from the baroreceptors of blood vessels to the medulla oblongata from the aortic arch and carotid sinus. Breathing also affects the tone of the vagus nerves. In connection with breathing - respiratory arrhythmia, when the heart slows down during exhalation.

    The tone of the sympathetic nerves of the heart at rest is weakly expressed. If you cut the sympathetic nerves, the frequency of contractions decreases by 6-10 beats per minute. This tone increases with physical activity and increases with various diseases. The tone is well expressed in children and newborns (129-140 beats per minute)

    The heart is still susceptible to the action of a humoral factor- hormones (adrenal glands - adrenaline, norepinephrine, thyroid gland - thyroxine and the mediator acetylcholine)

    Hormones have a + effect on all 4 properties of the heart. The heart is affected by the electrolyte composition of the plasma and cardiac function changes when the concentration of potassium and calcium changes. Hyperkalemia- increased potassium levels in the blood are a very dangerous condition; this can lead to cardiac arrest in diastole. Hypokalimi I - a less dangerous condition on the cardiogram is a change in the PQ distance, distortion of the T wave. The heart stops in systole. Body temperature also affects the heart - an increase in body temperature by 1 degree - an increase in heart function - by 8-10 beats per minute.

    Systolic volume

    1. Preload (the degree of stretching of cardiomyocytes before their contraction. The degree of stretching will be determined by the volume of blood that will be in the ventricles.)
    2. Contractility (Stretching of cardiomyocytes, where the length of the sarcomere changes. Typically, the thickness is 2 µm. The maximum force of contraction of cardiomyocytes is up to 2.2 µm. This is the optimal ratio between the myosin bridges and actin filaments, when their interaction is maximum. This determines the force of contraction, further stretching up to 2.4 reduces contractility. This adapts the heart to the blood flow, with its increase - a greater force of contraction. The force of contraction of the myocardium can change without changing the amount of blood, due to the hormones adrenaline and norepinephrine, calcium ions, etc. - the force of contraction of the myocardium increases)
    3. Afterload (Afterload is the myocardial tension that must occur in systole for the semilunar valves to open. The amount of afterload is determined by the value of systolic pressure in the aorta and pulmonary trunk)

    Laplace's law

    Degree of ventricular wall stress = Intragastric pressure * radius / wall thickness. The greater the intraventricular pressure and the larger the radius (the size of the lumen of the ventricle), the greater the stress of the ventricular wall. An increase in thickness has an inversely proportional effect. T=P*r/W

    The amount of blood flow depends not only on minute volume, but it is also determined by the amount of peripheral resistance that occurs in the vessels.

    Blood vessels have a powerful influence on blood flow. All blood vessels are lined with endothelium. Next is the elastic framework, and in the muscle cells there are also smooth muscle cells and collagen fibers. The vascular wall obeys Laplace's law. If there is intravascular pressure inside a vessel and the pressure causes stretching in the wall of the vessel, then there is a state of tension in the wall. The radius of the vessels also affects. The voltage will be determined by the product of pressure and radius. In the vessels we can distinguish the basal vascular tone. Vascular tone, which is determined by the degree of contraction.

    Basal tone- determined by the degree of stretching

    Neurohumoral tone- influence of nervous and humoral factors on vascular tone.

    An increased radius puts more stress on the walls of blood vessels than in a can, where the radius is smaller. In order for normal blood flow to occur and adequate blood supply to be ensured, there are vascular regulation mechanisms.

    They are represented by 3 groups

    1. Local regulation of blood flow in tissue
    2. Nervous regulation
    3. Humoral regulation

    Tissue blood flow provides

    Delivery of oxygen to cells

    Delivery of nutrients (glucose, amino acids, fatty acids, etc.)

    CO2 removal

    Removal of H+ protons

    Regulation of blood flow- short-term (several seconds or minutes as a result of local changes in tissues) and long-term (occurs over hours, days and even weeks. This regulation is associated with the formation of new vessels in tissues)

    The formation of new vessels is associated with an increase in tissue volume and an increase in the metabolic rate in the tissue.

    Angeogenesis- formation of blood vessels. This occurs under the influence of growth factors - vascular endothelial growth factor. Fibroblast growth factor and angiogenin

    Humoral regulation of blood vessels

    1. 1. Vasoactive metabolites

    A. Vasodilation is provided by - decrease in pO2, increase - CO2, t, K+ lactic acid, adenosine, histamine

    b.vasoconstriction is caused by an increase in serotonin and a decrease in temperature.

    2. Influence of the endothelium

    Endothelins (1,2,3). - narrowing

    Nitric oxide NO - expansion

    Formation of nitric oxide (NO)

    1. Release of Ach, bradykinin
    2. Opening of Ca+ channels in the endothelium
    3. Ca+ binding to calmodulin and its activation
    4. Activation of enzyme (nitric oxide synthetase)
    5. Conversion of L fringine to NO

    Mechanism of actionNO

    NO - activates guanyl cyclase GTP - cGMP - opening of K channels - release of K + - hyperpolarization - decrease in calcium permeability - dilation of smooth muscles and dilation of blood vessels.

    Has a cytotoxic effect on bacteria and tumor cells when isolated from leukocytes

    Is a mediator of excitation transmission in some neurons of the brain

    Mediator of parasympathetic postganglionic fibers for penile vessels

    Possibly involved in the mechanisms of memory and thinking

    A. Bradikinin

    B. Callidin

    Kininogen with WWII - bradykinin (with Plasma kallikrein)

    Kininogen with YVD - kallidin (with tissue kallikrein)

    Kinins are formed during the active activity of the sweat glands, salivary glands and pancreas.

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