Regulation of blood pressure. Increased blood pressure. Regulation of vascular tone. Regulation of systemic blood pressure

Blood pressure is a variable value that is influenced by both internal and external factors.

Unlike healthy people, patients suffering from hypertension have pathological changes in the activity of regulatory systems that maintain constant internal environment body.

Nature has given man natural mechanisms to maintain balance in the body. The mechanism of blood pressure regulation is very complex. It is enough to indicate such components as the central nervous system, the sympathetic and parasympathetic divisions of the autonomic nervous system, endocrine system, receptors located in the aortic arch, and receptors at the branching site of the carotid arteries (carotid sinus).

The sympathetic division of the autonomic nervous system influences blood pressure levels with the help of mediators (special protein substances - catecholamines) adrenaline and norepinephrine. These substances are produced by the adrenal glands; and their release into the blood is accompanied by increased heart rate and vasospasm. Physical exercise, anxiety, and poor lifestyle contribute to the activation of systems in the body (pressor systems) responsible for increasing blood pressure. But at the same time, provision is made for the inclusion of systems responsible for lowering blood pressure (depressor systems), primarily steam sympathetic division autonomic nervous system. And its mediator acetylcholine, which can slow down the pulse and dilate peripheral blood vessels.

Particular attention should be paid to the role of the kidneys, both in increasing and normalizing blood pressure.

On the one hand, as a result of the sympathetic influence of catecholamines and a decrease in blood supply to the kidneys, another powerful pressor mechanism, renin, is triggered, leading to the formation of the active substance angiotensin-2, which has a powerful vasoconstrictor effect, which increases the overall peripheral vascular resistance. The load on the heart muscle under the influence of these factors increases many times, which can lead to thickening of the wall of the left ventricle of the heart (hypertrophy).

AH is accompanied structural changes heart and blood vessels. Complications of the disease are a consequence of these pathological changes. That is why, in addition to effective blood pressure control, drugs that lower blood pressure should act on the process of remodeling (reducing pathological processes in the heart and blood vessels).

The level of renin in blood plasma depends on factors such as gender, age, time of day, etc. It can be higher in morning hours. In women it is lower than in men; in both sexes it decreases with age.

Together, renin and angiotensin-2 stimulate the production of adrenal glands important hormone aldosterone, which delays the release of sodium from the body and removes potassium more strongly. Aldosterone regulates the reabsorption (reabsorption) of sodium in lower parts renal tubules. It also promotes the redistribution of calcium and sodium from the cellular space into the cells, increasing permeability cell membranes. In the muscle fibers of the walls of peripheral arteries, the concentration of sodium and calcium increases significantly. Sodium intensively attracts water after itself. Swelling occurs vascular wall and narrowing of the lumen of blood vessels. This is accompanied by an increase in resistance to blood flow and an increase in diastolic blood pressure. In addition, sodium retention in the arterial walls increases the sensitivity of the receptors embedded in them to pressor substances circulating in the blood (renin and angiotensin-2). All this contributes to increased vascular tone, as one of the components in the overall picture of high blood pressure.

On the other hand, the role of the kidneys is great as an organ that lowers blood pressure, since the cells of the medulla of the kidneys synthesize active substances kinins and prostaglandins, which have a powerful vasodilatory effect that reduces peripheral resistance. The concentration of kinins in the blood of patients in initial stage arterial hypertension increases significantly, which is considered as a compensatory reaction of the body to increased activity of the pressor systems. As hypertension progresses, the depressor capabilities of the kidneys.

Pressor substances become depleted and begin to predominate. Blood pressure becomes higher and more persistent.

Prostaglandins of the E series are formed in the medulla of the kidneys and are capable of dilating blood vessels, increasing renal blood flow, removing excess sodium from the body through the kidneys and, very importantly, actively removing sodium from the kidneys. muscle fibers arterial walls, thereby reducing their swelling and reducing sensitivity to substances that constrict blood vessels. This leads to a decrease in blood pressure. With a long course of hypertension as atherosclerosis of the renal vessels increases, as well as in patients with chronic kidney diseases, as the renal tissue dies and decreases, the production of prostaglandin decreases and the depressor function of the kidneys is depleted, which explains the development of stable and high level hypertension.

Many medications are able to reduce the body’s own compensatory functions aimed at lowering and stabilizing blood pressure.

These are non-steroidal anti-inflammatory drugs (diclofenac, indomethacin, butadione, etc.) and their combinations. An increase in blood pressure can be caused by regular use of analgesics (trigan, analgin, etc.), corticosteroid hormones and contraception containing artificial estrogens.

The reserves of the complex regulatory mechanism in the body are purely individual, and if they continue long time If unfavorable factors act, the depressor systems become depleted. Persistent changes (pathology) appear in the body, in in this case persistent increase in blood pressure. The ability to measure blood pressure is an important step in disease control, but you should not stop there.

Blood pressure is regulated by short-, medium- and long-term adaptive reactions carried out by complex nervous, humoral and renal mechanisms.

A. Short-term regulation.

Immediate reactions that ensure continuous regulation of blood pressure are mediated mainly by reflexes of the autonomic nervous system. Changes in blood pressure are perceived both in the central nervous system (hypothalamus and brain stem) and in the periphery by specialized sensors (baroreceptors). Reducing blood pressure increases sympathetic tone, increases the secretion of adrenaline by the adrenal glands and suppresses the activity of the vagus nerve. The result is vasoconstriction of blood vessels great circle blood circulation, heart rate and contractility of the heart increases, which is accompanied by an increase in blood pressure. Arterial hypertension, on the contrary, inhibits sympathetic impulses and increases the tone of the vagus nerve.

Peripheral baroreceptors are located in the common bifurcation area carotid artery and in the aortic arch. An increase in blood pressure increases the frequency of baroreceptor impulses, which inhibits sympathetic vasoconstriction and increases the tone of the vagus nerve (baroreceptor reflex). A decrease in blood pressure leads to a decrease in the frequency of baroreceptor impulses, which causes vasoconstriction and reduces the tone of the vagus nerve. Carotid baroreceptors send afferent impulses to the vasomotor centers in the medulla oblongata along Hering's nerve (branch glossopharyngeal nerve). From the baroreceptors of the aortic arch, afferent impulses arrive along vagus nerve. The physiological significance of carotid baroreceptors is greater than that of aortic ones, because they ensure blood pressure stability during sudden functional changes (for example, when changing body position). Carotid baroreceptors are better adapted to perceive blood pressure in the range from 80 to 160 mm Hg. Art. Adaptation to sudden changes in blood pressure develops over the course of

1-2 days; therefore, this reflex is ineffective from the point of view of long-term regulation.

All inhalational anesthetics suppress the physiological baroreceptor reflex, the weakest inhibitors being isoflurane and desflurane. Stimulation of cardiopulmonary stretch receptors located in the atria and pulmonary vessels can also cause vasodilation.

B. Medium-term regulation. Arterial hypotension persisting for several minutes, in combination with increased sympathetic impulses, leads to activation of the re-nin-angiotensin-aldosterone system (Chapter 31), an increase in the secretion of antidiuretic hormone (ADH, synonym - arginine-vasopressin) and a change in transcapillary fluid exchange (chapter 28). AH-giotensin II and ADH are powerful arteriolar vasoconstrictors. Their immediate effect is to increase OPSS. For the secretion of ADH in an amount sufficient to ensure vasoconstriction, a greater decrease in blood pressure is required than for the corresponding effect of angiotensin P to appear.

Sustained changes in blood pressure affect fluid exchange in tissues due to changes in pressure in the capillaries. Arterial hypertension causes the movement of fluid from blood vessels into the interstitium, arterial hypotension - in the opposite direction. Compensatory changes in BCC help reduce blood pressure fluctuations, especially with renal dysfunction.

B. Long-term regulation. The influence of slow-acting renal regulatory mechanisms is manifested in cases where a stable change in blood pressure persists for several hours. Normalization of blood pressure by the kidneys is carried out by changing the sodium and water content in the body. Hypotension results in sodium (and water) retention, while hypertension increases sodium excretion.

More on the topic Blood pressure regulation:

1. Dysfunction of blood pressure regulation mechanisms
2. 23.BLOOD PRESSURE. DETERMINATION METHOD (N.S. KOROTKOV). BLOOD PRESSURE IN NORMAL AND IN PATHOLOGY. DIAGNOSTIC VALUE

After we found out the classification and normal numbers blood pressure, one way or another it is necessary to return to issues of circulatory physiology. Blood pressure healthy person, despite significant fluctuations depending on physical and emotional stress, as a rule, is maintained at a relatively stable level. This is facilitated by complex mechanisms nervous and humoral regulation who seek to return blood pressure to its original level after the end of the provoking factors. Maintaining blood pressure at a constant level is ensured by the coordinated functioning of the nervous and endocrine systems, as well as the kidneys.

All known pressor (increasing pressure) systems, depending on the duration of the effect, are divided into systems:

• rapid response (baroreceptors of the sinocarotid zone, chemoreceptors, sympathoadrenal system) - begins in the first seconds and lasts several hours;
• medium duration (renin-angiotensin) - turns on after a few hours, after which its activity can be either increased or decreased;
• long-acting (sodium-volume-dependent and aldosterone) - can act for a long time.

All mechanisms are, to a certain extent, involved in regulating the activity of the circulatory system, both under natural loads and under stress. Activity internal organs- brain, heart and others in high degree depends on their blood supply, for which it is necessary to maintain blood pressure in the optimal range. That is, the degree of increase in blood pressure and the rate of its normalization must be adequate to the degree of load.

When blood pressure is too low, a person is prone to fainting and loss of consciousness. This is due to insufficient blood supply to the brain. In the human body, there are several systems for monitoring and stabilizing blood pressure, which mutually support each other. The nervous mechanisms are represented by the autonomic nervous system, the regulatory centers of which are located in the subcortical areas of the brain and are closely connected with the so-called vasomotor center of the medulla oblongata.

These centers receive the necessary information about the state of the system from a kind of sensors - baroreceptors located in the walls of large arteries. Baroreceptors are located primarily in the walls of the aorta and carotid arteries, which supply blood to the brain. They react not only to the value of blood pressure, but also to the rate of its increase and amplitude pulse pressure. Pulse pressure is a calculated indicator that means the difference between systolic and diastolic blood pressure. Information from the receptors travels along the nerve trunks to the vasomotor center. This center controls arterial and venous tone, as well as the strength and frequency of heart contractions.

When deviating from standard values, for example, when blood pressure decreases, the cells of the center send a command to the sympathetic neurons, and the tone of the arteries increases. The baroreceptor system is one of the fast-acting regulatory mechanisms; its effect is manifested within a few seconds. The power of regulatory influences on the heart is so great that severe irritation baroreceptor zone, for example, with a sharp blow to the area of ​​the carotid arteries can cause short stop heart and loss of consciousness due to sharp fall Blood pressure in the vessels of the brain. The peculiarity of baroreceptors is their adaptation to a certain level and range of blood pressure fluctuations. The phenomenon of adaptation is that receptors respond to changes in the usual pressure range less strongly than to changes of the same magnitude in an unusual blood pressure range. Therefore, if for any reason the blood pressure level remains persistently elevated, the baroreceptors adapt to it and their activation level decreases (this blood pressure level is already considered normal). This kind of adaptation occurs with arterial hypertension, and is caused by the use of medications sharp a decrease in blood pressure will already be perceived by baroreceptors as a dangerous decrease in blood pressure with subsequent activation of counteraction to this process. When the baroreceptor system is artificially switched off, the range of blood pressure fluctuations during the day increases significantly, although on average it remains in the normal range (due to the presence of other regulatory mechanisms). In particular, the action of the mechanism that monitors the sufficient supply of brain cells with oxygen is realized just as quickly.

For this purpose, there are special sensors in the brain vessels that are sensitive to oxygen tension in arterial blood- chemoreceptors. Since most common cause a decrease in oxygen tension serves as a decrease in blood flow due to a decrease in blood pressure, a signal from chemoreceptors is sent to the higher sympathetic centers, which can increase the tone of the arteries and also stimulate the work of the heart. Thanks to this, blood pressure is restored to the level necessary to supply blood to brain cells.

The third mechanism, sensitive to changes in blood pressure, acts more slowly (over several minutes) - the renal mechanism. Its existence is determined by the operating conditions of the kidneys, which require maintaining stable blood pressure for normal blood filtration. renal arteries. For this purpose, the so-called juxtaglomerular apparatus (JGA) functions in the kidneys. When pulse pressure decreases due to one reason or another, ischemia of the JGA occurs and its cells produce their hormone - renin, which is converted in the blood into angiotensin-1, which in turn, thanks to the angiotensin-converting enzyme (ACE), is converted into angiotensin-2, which has a strong vasoconstrictor effect, and blood pressure rises.

The renin-angiotensin system (RAS) regulation does not react as quickly and accurately as the nervous system, and therefore even a short-term decrease in blood pressure can trigger the formation significant amount angiotensin-2 and thereby cause a sustained increase in arterial tone. In this regard, a significant place in the treatment of diseases of cardio-vascular system belongs to drugs that reduce the activity of the enzyme that converts angiotensin-1 into angiotensin-2. The latter, acting on the so-called type 1 angiotensin receptors, has many biological effects.

• Peripheral vasoconstriction
• Aldosterone release
• Synthesis and release of catecholamines
• Control of glomerular circulation
• Direct antinatriuretic effect
• Stimulation of hypertrophy of vascular smooth muscle cells
• Stimulation of cardiomyocyte hypertrophy
• Stimulation of development connective tissue(fibrosis)

One of them is the release of aldosterone by the adrenal cortex. The function of this hormone is to reduce the excretion of sodium and water in the urine (antinatriuretic effect) and, accordingly, to retain them in the body, that is, to increase circulating blood volume (CBV), which also increases blood pressure.

Renin-angiotensin system (RAS)

RAS, the most important among humoral endocrine systems regulating blood pressure, which affects two main determinants of blood pressure - peripheral resistance and circulating blood volume. There are two types of this system: plasma (systemic) and tissue. Renin is secreted by the UGA of the kidneys in response to a decrease in pressure in the afferent arteriole of the glomeruli of the kidneys, as well as a decrease in sodium concentration in the blood.

ACE plays the main role in the formation of angiotensin 2 from angiotensin 1; there is another, independent pathway for the formation of angiotensin 2 - the non-circulating “local” or tissue renin-angiotensin paracrine system. It is found in the myocardium, kidneys, vascular endothelium, adrenal glands and nerve ganglia and is involved in the regulation of regional blood flow. The mechanism of formation of angiotensin 2 in this case is associated with the action of the tissue enzyme - chymase. As a result, efficiency may decrease ACE inhibitors, which do not affect this mechanism of angiotensin 2 formation. It should also be noted that the level of activation of the circulating RAS does not have a direct connection with an increase in blood pressure. In many patients (especially the elderly), plasma renin and angiotensin 2 levels are quite low.

Why, after all, does hypertension occur?

In order to understand this, you need to imagine that in the human body there is a kind of scale on one side of which there are pressor (that is, increasing blood pressure) factors, on the other - depressor (lowering blood pressure).

When pressor factors outweigh, pressure increases; when depressor factors outweigh, pressure decreases. And normally, in humans, these scales are in dynamic equilibrium, due to which the pressure is maintained at a relatively constant level.

What is the role of adrenaline and norepinephrine in the development of arterial hypertension?

The greatest importance in the pathogenesis of arterial hypertension is given to humoral factors. Has powerful direct pressor and vasoconstrictor activity catecholamines - adrenaline and norepinephrine, which are produced mainly in the adrenal medulla. They are also neurotransmitters of the sympathetic division of the autonomic nervous system. Norepinephrine acts on the so-called alpha-adrenergic receptors and acts for quite a long time. Mainly peripheral arterioles narrow, which is accompanied by an increase in both systolic and diastolic blood pressure. Adrenaline, stimulating alpha and beta adrenergic receptors (b1 - cardiac muscle and b2 - bronchi), intensively but briefly increases blood pressure, increases blood sugar, increases tissue metabolism and the body's need for oxygen, and leads to an acceleration of heart contractions.

The effect of table salt on blood pressure

Kitchen or salt in excess quantities increases the volume of extracellular and intracellular fluid, causes swelling of the arterial wall, thereby contributing to the narrowing of their lumen. Increases the sensitivity of smooth muscles to pressor substances and causes an increase in total peripheral vascular resistance (TPVR).

What are the current hypotheses for the occurrence of arterial hypertension?

Currently, this point of view is accepted - the reason for the development of the primary (essential) is the complex impact various factors which are listed below.

Unmodifiable:

• age (2/3 of people over 55 years of age have hypertension, and if blood pressure is normal, the probability of developing it in the future is 90%)
• hereditary predisposition (up to 40% of cases of hypertension)
• intrauterine development (low birth weight). Except increased risk development of hypertension, as well as the risk of metabolic abnormalities associated with hypertension: insulin resistance, diabetes, hyperlipidemia, abdominal type obesity.

Modifiable lifestyle factors (80% of hypertension is associated with these factors):

• smoking,
• unhealthy diet (overeating, low content potassium, high content salt and animal fats, low content of dairy products, vegetables and fruits),
• overweight and obesity (body mass index more than 25 kg/m2, central type of obesity - waist size in men more than 102 cm, among women more than 88 cm),
• psychosocial factors (moral and psychological climate at work and at home),
• high level of stress,
• alcohol abuse,
• low level of physical activity.

In order for the mechanisms that regulate blood pressure to adequately respond to the needs of the body, they must receive information about these needs.

This function is performed by chemoreceptors. Chemoreceptors respond to a lack of oxygen in the blood, an excess of carbon dioxide and hydrogen ions, and a shift in the blood reaction (blood pH) to the acidic side. Chemoreceptors are found throughout the vascular system. There are especially many of these cells in the common carotid artery and in the aorta.

A lack of oxygen in the blood, an excess of carbon dioxide and hydrogen ions, and a shift in blood pH to the acidic side excite chemoreceptors. Impulses from chemoreceptors nerve fibers enter the vasomotor center of the brain (VDC). SDC consists of nerve cells(neurons) that regulate vascular tone, strength, heart rate, volume of circulating blood, that is, blood pressure. The SDC neurons exert their influence on vascular tone, the strength and frequency of heart contractions, and the volume of circulating blood through the neurons of the sympathetic and parasympathetic autonomic nervous system (ANS), which directly affect vascular tone, the strength and frequency of heart contractions.

The SDC consists of pressor, depressor and sensory neurons. An increase in the excitation of pressor neurons increases the excitation (tone) of the neurons of the sympathetic ANS and reduces the tone of the parasympathetic ANS. This leads to an increase in vascular tone (vascular spasm, reduction in the lumen of blood vessels), to an increase in the strength and frequency of heart contractions, that is, to an increase in blood pressure. Depressor neurons reduce the excitation of pressor neurons and, thus, indirectly contribute to vasodilation (decreasing vascular tone), reduce the strength and frequency of heart contractions, that is, lower blood pressure.

Sensory (sensitive) neurons, depending on the information received from the receptors, have an excitatory effect on the pressor or depressor neurons of the SDC.

The functional activity of pressor and depressor neurons is regulated not only by sensory neurons of the SDC, but also by other neurons of the brain. Indirectly through the hypothalamus, neurons of the motor zone of the cerebral cortex have an excitatory effect on pressor neurons.

Neurons of the cerebral cortex influence the SDC through neurons of the hypothalamic region.

Strong emotions: anger, fear, anxiety, excitement, great joy, grief can cause excitation of the pressor neurons of the SDC. Pressor neurons excite on their own if they are in a state of ischemia (a state of insufficient oxygen supply to them with the blood). In this case, blood pressure rises very quickly and very strongly. The fibers of the sympathetic ANS are densely entwined with blood vessels, the heart, and end with numerous branches in various organs and tissues of the body, including those near cells called transducers. These cells, in response to an increase in the tone of the sympathetic ANS, begin to synthesize and release substances into the blood that affect the increase in blood pressure.

Transducers are:

• 1. Chromaffin cells of the adrenal medulla;
• 2. Juxt-glomerular cells of the kidneys;
• 3. Neurons of the hypothalamic supraoptic and paraventricular nuclei.

Chromaffin cells of the adrenal medulla.

These cells, with an increase in the tone of the sympathetic ANS, begin to synthesize and release hormones into the blood: adrenaline and norepinephrine. These hormones in the body have the same effects as the sympathetic ANS. In contrast to the influence of the sympathetic ANS system, the effects of adrenaline and norepinephrine in the adrenal glands are more prolonged and widespread.

Juxt-glomerular cells of the kidneys.

These cells, with an increase in the tone of the sympathetic ANS, as well as during renal ischemia (a state of insufficient supply of oxygen to the kidney tissues with the blood), begin to synthesize and release the proteolytic enzyme renin into the blood.

Renin in the blood breaks down another protein, angiotensinogen, to form the protein angiotensin 1. Another enzyme in the blood, ACE (Angiotensin Converting Enzyme), breaks down angiotensin 1 to form the protein angiotensin 2.

Angiotensin 2:

• - has a very strong and long-lasting vasoconstrictive effect on blood vessels. Angiotensin 2 exerts its effect on blood vessels through angiotensin receptors (AT);
• - stimulates the synthesis and release into the blood cells zona glomerulosa adrenal glands aldosterone, which retains sodium, and, therefore, water in the body. This leads to: an increase in the volume of circulating blood, sodium retention in the body leads to the fact that sodium penetrates into the endothelial cells covering blood vessels from the inside, carrying water with it inside the cell. Endothelial cells increase in volume. This leads to a narrowing of the lumen of the vessel. Reducing the lumen of the vessel increases its resistance. An increase in vascular resistance increases the strength of heart contractions. Sodium retention increases the sensitivity of angiotensin receptors to angiotensin 2. This accelerates and enhances the vasoconstrictor effect of agiotensin 2;
• - stimulates the cells of the hypothalamus to synthesize and release into the blood the antidiuretic hormone vasopressin and the cells of the adenohypophysis of adrenocorticotropic hormone (ACTH). ACTH stimulates the synthesis of glucocorticoids by cells of the zona fasciculata of the adrenal cortex. The largest biological effect has cortisol. Cortisol potentiates an increase in blood pressure.

All this, in particular and in total, leads to an increase in blood pressure. Neurons of the hypothalamic supraoptic and paraventricular nuclei synthesize antidiuretic hormone vasopressin. Through their processes, neurons release vasopressin into the posterior lobe of the pituitary gland, from where it enters the blood. Vasopressin has a vasoconstrictor effect, retaining water in the body.

This leads to an increase in circulating blood volume and an increase in blood pressure. In addition, vasopressin enhances the vasoconstrictor effects of adrenaline, norepinephrine and angiotensin 2.

Information about the volume of circulating blood and the strength of heart contractions comes to the SDC from baroreceptors and receptors low pressure. Baroreceptors are branches of the processes of sensory neurons in the wall of arterial vessels. Baroreceptors convert stimulation from stretching of the vessel wall into nerve impulse. Baroreceptors are found throughout the vascular system.

Their greatest number is in the aortic arch and carotid sinus. Baroreceptors are stimulated by stretch. An increase in the force of heart contractions increases the stretching of the walls of arterial vessels at the locations of the baroreceptors. The excitation of baroreceptors increases in direct proportion to the increase in the strength of heart contractions. The impulse from them goes to the sensory neurons of the SDC. The sensory neurons of the SDC excite the depressor neurons of the SDC, which reduce the excitation of the pressor neurons of the SDC. This leads to a decrease in the tone of the sympathetic ANS and an increase in the tone of the parasympathetic ANS, which leads to a decrease in the strength and frequency of heart contractions, vasodilation, that is, to a decrease in blood pressure. On the contrary, the decrease in the strength of heart contractions is lower normal indicators reduces the excitation of baroreceptors, reduces impulses from them to the sensory neurons of the SDC. In response to this, the sensory neurons of the SDC excite the pressor neurons of the SDC.

This leads to an increase in the tone of the sympathetic ANS and a decrease in the tone of the parasympathetic ANS, which leads to an increase in the strength and frequency of heart contractions, vasoconstriction, that is, to an increase in blood pressure. In the walls of the atria and pulmonary artery There are low pressure receptors that are excited when blood pressure decreases due to a decrease in circulating blood volume.

With blood loss, the volume of circulating blood decreases and blood pressure decreases. Excitation of baroreceptors decreases, and excitation of low pressure receptors increases.

This leads to an increase in blood pressure. As blood pressure approaches normal, excitation of baroreceptors increases, and excitation of low pressure receptors decreases.

This prevents blood pressure from increasing above normal. In case of blood loss, restoration of the volume of circulating blood is achieved by the transition of blood from the depot (spleen, liver) into the bloodstream. Note: About 500 ml is deposited in the spleen. blood, and in the liver and in the vessels of the skin there is about 1 liter of blood.

The volume of circulating blood is controlled and maintained by the kidneys through the production of urine. When systolic blood pressure is less than 80 mm. Hg Art. urine is not formed at all, with normal blood pressure - normal urine formation, with increased blood pressure, urine is formed in direct proportion to more (hypertensive diuresis). At the same time, sodium excretion in the urine increases (hypertensive natriuresis), and water is also excreted along with sodium.

When the volume of circulating blood increases above normal, the load on the heart increases. In response to this, atrial cardiomycytes respond by synthesizing and releasing a protein into the blood - atrial natriuretic peptide (ANP), which increases the excretion of sodium and, therefore, water in the urine. The cells of the body can themselves regulate the supply of oxygen to them with the blood and nutrients.

Under conditions of hypoxia (ischemia, insufficient oxygen supply), cells secrete substances (for example, adenosine, nitric oxide NO, prostacyclin, carbon dioxide, adenosine phosphates, histamine, hydrogen ions (lactic acid), potassium ions, magnesium ions) that dilate the adjacent arterioles , thereby increasing the flow of blood, and, accordingly, oxygen and nutrients.

In the kidneys, for example, during ischemia, the cells of the renal medulla begin to synthesize and release kinins and prostaglandins into the blood, which have a vasodilating effect. As a result - arterial vessels the kidneys expand, the blood supply to the kidneys increases. Note: with excess salt intake from food, the synthesis of kinins and prostaglandins by kidney cells decreases.

Blood rushes primarily to where the arterioles are more dilated (to the place of least resistance). Chemoreceptors trigger a mechanism to increase blood pressure in order to speed up the delivery of oxygen and nutrients to cells, which the cells lack. As the ischemic state is resolved, the cells stop releasing substances that dilate adjacent arterioles, and the chemoreceptors stop stimulating an increase in blood pressure.

Additional information block:

Functional parameters of blood circulation are constantly captured by receptors located in various parts of the cardiovascular system. Afferent impulses from these receptors enter the vasomotor centers of the medulla oblongata. These centers send signals along efferent fibers to the effectors - the heart and blood vessels. The main mechanisms of general cardiovascular regulation are aimed at maintaining pressure in the vascular system , necessary for normal blood flow. This is accomplished through combined changes in total peripheral resistance and cardiac output.

BP = MOC x OPSS

IOC- minute volume of blood circulation

SV = SV (stroke volume) x heart rate

SVD depends on venous return and myocardial contractility

OPSS- total peripheral vascular resistance

OPSS depends on blood viscosity and vessel radius.

Depending on the speed of development adaptive processes all regulatory mechanisms hemodynamics can be divided into three groups:

1) mechanisms of short-term action;

2) mechanisms of intermediate (in time) action;

3) long-acting mechanisms.

Short-term regulatory mechanisms

These mechanisms include predominantly vasomotor reactions of nervous origin.:

These impulses have an inhibitory effect on the sympathetic centers and an exciting effect on the parasympathetic ones. As a result, vascular tone decreases , as well as the frequency and strength of heart contractions. Both lead to a decrease in blood pressure. When pressure drops, impulses from baroreceptors decrease, and reverse processes develop, ultimately leading to an increase in pressure.

2) chemoreceptor reflexes;

Renal fluid volume control system

Increased blood pressure has several main consequences:

1) the excretion of fluid by the kidneys increases;

2) as a result of increased fluid excretion, the volume of extracellular fluid decreases and, therefore,

3) blood volume decreases;

4) a decrease in blood volume leads to a decrease in blood pressure.

When blood pressure falls, reverse processes occur: renal excretion decreases, blood volume increases, venous return and cardiac output increase and blood pressure rises again.

Effects of vasopressin. Vasopressin, or anti-diuretic hormone (ADH), in the middle and high doses has a vasoconstrictor effect, most pronounced at the level of arterioles. However, the main effect of this hormone is the regulation of water reabsorption in the distal tubules of the kidneys. By influencing the release of water, vasopressin affects blood pressure.

Effects of Aldosterone. Aldosterone is a hormone of the adrenal cortex that affects kidney function. Aldosterone, affecting the renal tubules, retains sodium in the body and, as a result, water. Excessive production of aldosterone leads to significant; water and salt retention and hypertension. With reduced aldosterone production, hypotension is observed.

Thus, against violations blood pressure And blood volume Three “lines of defense” are constantly operating, each at its own time (in terms of beginning and duration). With short-term fluctuations in pressure and blood volume, vascular reactions are activated, while with long-term changes, compensatory changes in blood volume predominate. IN the latter case first, the content of water and electrolytes in the blood changes, and if necessary (in different terms) shifts also occur in the content of plasma proteins and cellular elements.

Questions for independent extracurricular work of students:

1. Characteristics of blood pressure as a plastic constant of the body.

2. Factors that determine blood pressure levels.

3. Characteristics of the receptor apparatus, centers and actuators of the functional system of blood pressure regulation: mechanisms of short-term, intermediate, long-term regulation of blood pressure.

• Analyze the functional system for maintaining blood pressure. Redraw the diagram; on the FUS diagram, highlight the center of regulation and direct connections in red, and the receptors and feedback connections in blue.

Fig.8. Scheme of a functional system for maintaining blood pressure at a level optimal for metabolism.

• Make a table in writing on the analysis of mechanisms of blood pressure regulation:

1. Lecture material.
2. Loginov A.V. Physiology with the basics of human anatomy. - M, 1983. - S. 192 - 198.
3. Normal physiology (Physiology course functional systems) / Ed. K.V. Sudakova. - M., 1999. - P.175-200.