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 vascular system. There are especially many of these cells in total 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 travel along nerve fibers to the vasomotor center of the brain (VMC). 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:
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:
All this, in particular and collectively, leads to an increase in blood pressure. Neurons of the hypothalamic supraoptic and paraventricular nuclei synthesize the 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 arterial vessels. Baroreceptors convert stimulation from the stretching of the vessel wall into a 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 and nutrients to them through the blood.
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, the arterial vessels of the kidneys dilate, and 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.
Arterial hypertension is a stable increase in blood pressure - systolic to a value > 140 mmHg Art. and/or diastolic to a level > 90 mm Hg. Art. according to at least double measurements using the method of N. S. Korotkov during two or more consecutive visits to the patient with an interval of at least 1 week.
Arterial hypertension is an important and pressing problem of modern health care. At arterial hypertension the risk of cardiovascular complications significantly increases, and it significantly reduces average life expectancy. High blood pressure is always associated with an increased risk of stroke, coronary heart disease, heart and kidney failure.
There are essential (primary) and secondary arterial hypertension. Essential arterial hypertension accounts for 90-92% (and according to some data 95%), secondary - about 8-10% of all cases of high blood pressure.
Blood pressure is formed and maintained at a normal level due to the interaction of two main groups of factors:
hemodynamic;
neurohumoral.
Hemodynamic factors directly determine the level of blood pressure, and the system of neurohumoral factors has a regulatory effect on hemodynamic factors, which allows keeping blood pressure within normal limits.
Hemodynamic factors that determine blood pressure
The main hemodynamic factors that determine blood pressure are:
minute blood volume, i.e. amount of blood, entering the vascular system in 1 minute; minute volume or cardiac output= stroke volume x number of heart contractions in 1 minute;
general peripheral resistance or patency of resistive vessels (arterioles and precapillaries);
elastic tension of the walls of the aorta and its large branches - general elastic resistance;
blood viscosity;
volume of circulating blood.
Neurohumoral systems of blood pressure regulation
Regulatory neurohumoral systems include:
rapid short-term action system;
system long acting(integrated control system).
Rapid short-acting system
The rapid short-acting system or adaptation system provides rapid control and regulation of blood pressure. It includes mechanisms for immediate regulation of blood pressure (seconds) and medium-term regulation mechanisms (minutes, hours).
Mechanisms of immediate blood pressure regulation
The main mechanisms of immediate blood pressure regulation are:
baroreceptor mechanism;
chemoreceptor mechanism;
ischemic reaction of the central nervous system.
Baroreceptor mechanism
The baroreceptor mechanism for regulating blood pressure functions as follows. With an increase in blood pressure and stretching of the artery wall, baroreceptors located in the area of the carotid sinus and aortic arch are excited, then information from these receptors enters the vasomotor center of the brain, from where impulses come, leading to a decrease in the influence of the sympathetic nervous system on the arterioles (they expand, decrease total peripheral vascular resistance - afterload), veins (venodilation occurs, cardiac filling pressure decreases - preload). Along with this, parasympathetic tone increases, which leads to a decrease in heart rate. Ultimately, these mechanisms lead to a decrease in blood pressure.
Chemoreceptor mechanism
Chemoreceptors involved in the regulation of blood pressure are located in the carotid sinus and aorta. The chemoreceptor system is regulated by blood pressure and the partial tension of oxygen and carbon dioxide in the blood. When blood pressure drops to 80 mm Hg. Art. and below, as well as with a decrease in the partial oxygen tension and an increase in carbon dioxide, chemoreceptors are excited, impulses from them enter the vasomotor center with a subsequent increase in sympathetic activity and arteriolar tone, which leads to an increase in blood pressure to normal levels.
Ischemic response of the central nervous system
This blood pressure regulation mechanism is activated when blood pressure drops rapidly to 40 mmHg. Art. and below. With such severe arterial hypotension, ischemia of the central nervous system and the vasomotor center develops, from which impulses to the sympathetic part of the autonomic nervous system increase, eventually vasoconstriction develops and blood pressure rises.
Medium-term mechanisms of arterial blood regulation pressure
Medium-term mechanisms of blood pressure regulation develop their action within minutes - hours and include:
renin-angiotensin system (circulating and local);
antidiuretic hormone;
capillary filtration.
Renin-angiotensin system
Both the circulating and local renin-angiotensin systems take an active part in the regulation of blood pressure. The circulating renin-angiotensin system leads to increased blood pressure as follows. In the juxtaglomerular apparatus of the kidneys, renin is produced (its production is regulated by the activity of baroreceptors of afferent arterioles and the influence of sodium chloride concentration on the macula densa in the ascending part of the nephron loop), under the influence of which angiotensin I is formed from angiotensinogen, which is converted under the influence of angiotensin-converting enzyme into angiotensin II, which has a pronounced vasoconstrictor effect and increases blood pressure. The vasoconstrictor effect of angiotensin II lasts from several minutes to several hours.
Antidiuretic hormone
Changes in the secretion of antidiuretic hormone by the hypothalamus regulate the level of blood pressure, and it is believed that the action of antidiuretic hormone is not limited only to the medium-term regulation of blood pressure, it also takes part in the mechanisms of long-term regulation. Under the influence of antidiuretic hormone, the reabsorption of water in the distal tubules of the kidneys increases, the volume of circulating blood increases, and the tone of the arterioles increases, which leads to an increase in blood pressure.
Capillary filtration
Capillary filtration takes a certain part in the regulation of blood pressure. With an increase in blood pressure, fluid moves from the capillaries into the interstitial space, which leads to a decrease in the volume of circulating blood and, accordingly, a decrease in blood pressure.
Long-acting arterial blood regulation system pressure
Activation of the long-acting (integral) blood pressure regulation system requires significantly more time (days, weeks) compared to the fast-acting (short-term) system. The long-acting system includes the following mechanisms for regulating blood pressure:
a) pressor volume-renal mechanism, functioning according to the scheme:
kidneys (renin) → angiotensin I → angiotensin II→ zona glomerulosa adrenal cortex (aldosterone) → kidneys (increased sodium reabsorption in the renal tubules) → sodium retention → water retention → increased circulating blood volume → increased blood pressure;
b) local renin-angiotensin system;
c) endothelial pressor mechanism;
d) depressor mechanisms (prostaglandin system, kallikreinin system, endothelial vasodilating factors, natriuretic peptides).
MEASUREMENT OF BLOOD PRESSURE WHEN EXAMINING A PATIENT WITH ARTERIAL HYPERTENSION
Measuring blood pressure using the auscultatory Korotkoff method is the main method for diagnosing arterial hypertension. To obtain numbers that correspond to true blood pressure, the following conditions and rules for measuring blood pressure must be observed.
Method of measuring blood pressure
Measurement conditions. Blood pressure measurement should be carried out in conditions of physical and emotional rest. Within 1 hour before measuring blood pressure, it is not recommended to drink coffee or eat food, smoking is prohibited, and physical activity is not allowed.
Position of the patient. Blood pressure is measured with the patient sitting or lying down.
Position of the tonometer cuff. The middle of the cuff placed on the patient's shoulder should be at the level of the heart. If the cuff is located below the level of the heart, blood pressure is overestimated; if higher, it is underestimated. The lower edge of the cuff should be 2.5 cm above the elbow, and a finger should fit between the cuff and the surface of the patient's shoulder. The cuff is placed on the bare arm - when measuring blood pressure through clothing, the readings are overestimated.
Stethoscope position. The stethoscope should fit snugly (but without compression!) to the surface of the shoulder in the place of the most pronounced pulsation of the brachial artery at the inner edge of the elbow.
Selecting the patient's hand for measuring blood pressure. When a patient first visits a doctor, blood pressure should be measured in both arms. Subsequently, blood pressure is measured on the arm with higher values. Normally, the difference in blood pressure on the left and right hand is 5-10 mmHg. Art. The higher difference may be due to anatomical features or pathology of the brachial artery itself of the right or left arm. Repeated measurements should always be taken on the same hand.
Elderly people also experience orthostatic hypotension Therefore, it is advisable to measure their blood pressure in the supine and standing positions.
Self-monitoring of blood pressure in an outpatient setting
Self-monitoring (measurement of blood pressure by the patient himself at home, in outpatient setting) is of great importance and can be performed using mercury, membrane, and electronic tonometers.
Self-monitoring of blood pressure allows you to establish the “white coat phenomenon” (an increase in blood pressure is registered only when visiting a doctor), make a conclusion about the behavior of blood pressure during the day and make a decision on the distribution of appointments antihypertensive drug within 24 hours, which can reduce the cost of treatment and increase its effectiveness.
24-hour blood pressure monitoring
Daily blood pressure monitoring is a repeated measurement of blood pressure during the day, carried out at certain intervals, most often in an outpatient setting (24-hour ambulatory blood pressure monitoring) or less often in a hospital in order to obtain a daily blood pressure profile.
Currently, 24-hour blood pressure monitoring is carried out, of course, non-invasively using various types of wearable automatic and semi-automatic monitor-recorder systems.
The following are installed benefits of 24-hour monitoring blood pressure compared to measuring it once or twice:
the ability to take frequent blood pressure measurements throughout the day and get a more accurate idea of the daily rhythm of blood pressure and its variability;
the ability to measure blood pressure in a normal, everyday environment familiar to the patient, which allows one to draw a conclusion about the true blood pressure characteristic of a given patient;
elimination of the “white coat” effect;
Under regulation of blood circulation understand its adaptation to changing functional activity and metabolic needs of organs and tissues, which is carried out in three main directions:
Q (or MOK)= V*S,
where V is the linear speed of blood flow; S is the cross-sectional area of the arterial vascular bed.
How the linear velocity of blood flow in systemic arterial vessels can be increased can be seen from the analysis of the following expressions. Previously, we presented one of the main expressions of hemodynamics:
MOK = (P 1 - P 2) / R
where P 1 is the average hemodynamic blood pressure in the aorta; P 2 - blood pressure at the mouth of the vena cava or in the right atrium; R is the total resistance to blood flow.
Since the blood pressure in the vena cava is close to zero, then P 1 - P 2 is actually equal to the average hemodynamic blood pressure at the beginning of the aorta. Because V * S = AD/R, it is possible to increase the linear speed of blood flow in arterial vessels with their relatively unchanged cross-sectional area by increasing blood pressure.
Arterial pressure blood depends mainly on the volume of blood volume, pumping function of the heart (MCF) and the value of the compulsory blood pressure. Thus, BP = IOC * OPS, so the increase at physical activity volume of blood pumped by the heart in 1 minute will be accompanied by an increase in blood pressure and an increase linear speed blood flow in arterial vessels. At the same time, the value of OPS has a very significant influence on the value of blood pressure and the speed of blood flow, which can vary over a wide range under the influence of blood pressure regulation mechanisms.
According to Poiseuille's law,
Where L- vessel length; η - blood viscosity; π - number equal to 3.14; r- radius of the vessel.
Since the numbers 8 And π are permanent L in an adult, blood viscosity changes little η is also a slightly changing value over a short period of time, then the value of peripheral resistance to blood flow is determined primarily by the radius of resistive vessels r. Resistance depends on the radius to the 4th power, so even small fluctuations in the radius of these vessels greatly affect the resistance to blood flow and its pressure in the arterial vessels.
It is obvious that the regulation of blood flow in the systemic arterial vessels and thereby in the entire vascular system depends on the value of the average hemodynamic blood pressure. Its increase is the most important driving force, accelerating blood flow in arterial vessels, and decreasing - slowing down blood flow. Thus, one of the main tasks of the mechanisms regulating blood flow in vessels is the regulation of blood pressure as the main force driving blood flow in the vessels.
Maintenance normal level blood pressure in main arteries is the most important condition necessary to ensure blood flow adequate to the needs of the body. Level regulation is carried out by a complex multi-circuit functional system, which uses the principles of pressure regulation based on deviation and (or) disturbance. Scheme of such a system, built on the basis of the principles of the theory functional systems PC. Anokhin, shown in Fig. 1. As in any other functional parameter regulation system internal environment body, it is possible to distinguish a regulated indicator, which is the level of blood pressure in the aorta, large arterial vessels and cavities of the heart.
Rice. 1. Scheme of the functional system for regulating blood pressure: 1-3 - impulses from extero-, intero-, proprioceptors
Direct assessment of blood pressure levels is carried out by baroreceptors of the aorta, arteries and heart. These receptors are mechanoreceptors, formed by the endings of afferent nerve fibers and respond to the degree of stretching by blood pressure of the walls of blood vessels and the heart by changing the number nerve impulses. The higher the pressure, the higher the frequency of nerve impulses generated in nerve endings forming baroreceptors. From receptors along afferent nerve fibers IX and X pairs cranial nerves streams of signals about the current value of blood pressure are transmitted to nerve centers regulating blood circulation. They receive information from chemoreceptors that control the tension of blood gases, from receptors in muscles, joints, tendons, as well as from exteroceptors. The activity of neurons in the centers that regulate blood pressure and blood flow also depends on the influence of the higher parts of the brain on them.
One of important functions of these centers is the formation of the level specified for regulation (setpoint) blood pressure. Based on a comparison of information about the magnitude of the current pressure entering the centers with its specified level for regulation, the nerve centers form a flow of signals transmitted to the effector organs. By changing their functional activity, you can directly influence the level of arterial blood pressure, adapting its value to the current needs of the body.
TO effector organs include: the heart, through the influence of which (stroke volume, heart rate, IOC), it is possible to influence the level of blood pressure; smooth myocytes vascular wall, through the influence on the tone of which it is possible to change the resistance of blood vessels to blood flow, blood pressure and blood flow in organs and tissues; kidneys, through influencing the processes of excretion and reabsorption of water in which it is possible to change the volume of circulating blood (CBV) and its pressure; blood depot, red Bone marrow, vessels of the microvasculature, in which, through the deposition, formation and destruction of red blood cells, the processes of filtration and reabsorption, it is possible to influence the bcc, its viscosity and pressure. Through the influence on these effector organs and tissues, the body's mechanisms of neurohumoral regulation (MHRR) can change blood pressure in accordance with the level set in the central nervous system, adapting it to the needs of the body.
The functional system of blood circulation regulation has various mechanisms of influence on the functions of effector organs and tissues. Among them are the mechanisms of the autonomic nervous system, adrenal hormones, using which you can change the functioning of the heart, the lumen (resistance) of blood vessels and influence blood pressure instantly (in seconds). In the functional system, signaling molecules (hormones, vasoactive substances of the endothelium and other nature) are widely used to regulate blood circulation. Their release and effect on target cells (smooth myocytes, renal tubular epithelium, hematopoietic cells, etc.) require tens of minutes, and changes in the volume of blood volume and its viscosity may require a longer time. Therefore, the speed of implementation of the influence on blood pressure levels is distinguished by the mechanisms of rapid response, medium-term response, slow response and long-term influence on blood pressure.
Rapid response mechanisms and quick influence changes in blood pressure are realized through the reflex mechanisms of the autonomic nervous system (ANS). Principles of construction neural pathways ANS reflexes are discussed in the chapter on the autonomic nervous system.
Reflex reactions to changes in blood pressure levels can change the value of blood pressure in seconds and thereby change the speed of blood flow in the vessels and transcapillary exchange. The mechanisms of rapid response and reflex regulation of blood pressure are activated when there is a sharp change in blood pressure, a change gas composition blood, cerebral ischemia, psycho-emotional arousal.
Any reflex is initiated by sending receptor signals to the reflex centers. Places of accumulation of receptors that respond to one type of influence are usually called reflexogenic zones. It has already been briefly mentioned that receptors that perceive changes in blood pressure are called baroreceptors or mechanoresisptorami stretching. They respond to fluctuations in blood pressure, causing greater or lesser stretching of the vessel walls, by changing the potential difference on the receptor membrane. The main number of baroreceptors is concentrated in the reflexogenic zones of large vessels and the heart. The most important of them for regulating blood pressure are the areas of the aortic arch and carotid sinus (the place where the common carotid artery branches into the internal and external carotid arteries). In these reflexogenic zones, not only baroreceptors are concentrated, but also chemoreceptors that perceive changes in the voltage of CO 2 (pCO 2) and 0 2 (pO 2,) in arterial blood.
Afferent nerve impulses arising in the receptor nerve endings are carried to the medulla oblongata. From the receptors of the aortic arch they go along the left depressor nerve, which in humans passes through the trunk of the vagus nerve (the right depressor nerve carries out impulses from receptors located at the beginning of the brachiocephalic truncus arteriosus). Afferent impulses from the carotid sinus receptors are carried out as part of a branch of the sinocarotid nerve, also called Hering's nerve(as part of the lingual pharyngeal nerve).
Vascular baroreceptors respond by changing the frequency of generation of nerve impulses to normal fluctuations in blood pressure levels. During diastole, when the pressure decreases (up to 60-80 mm Hg), the number of generated nerve impulses decreases, and with each ventricular systole, when the blood pressure in the aorta and arteries increases (up to 120-140 mm Hg), the frequency the impulses sent by these receptors to the medulla oblongata increase. The increase in afferent impulses progressively increases if blood pressure increases above normal. Afferent impulses from baroreceptors enter the neurons of the dentressor section of the circulatory center of the medulla oblongata and increase their activity. There are reciprocal relationships between the neurons of the depressor and pressor sections of this center, therefore, when the activity of the neurons of the depressor section increases, the activity of the neurons of the pressor section of the vasomotor center is inhibited.
The neurons of the pressor region send axons to the ireganglionic neurons of the sympathetic nervous system of the spinal cord, which innervate the vessels through the ganglion neurons. As a result of a decrease in the flow of nerve impulses to preganglionic neurons, their tone decreases and the frequency of nerve impulses sent by them to the ganglion neurons and further to the vessels decreases. The amount of norepinephrine released from postganglionic nerve fibers decreases, the vessels dilate and blood pressure decreases (Fig. 2).
In parallel with the initiation of reflex dilation of arterial vessels to increase blood pressure, rapid reflex inhibition of the pumping function of the heart develops. It occurs due to the sending of an increased flow of signals from baroreceptors along the afferent fibers of the vagus nerve to the neurons of the nerve nucleus. At the same time, the activity of the latter increases, and the flow of efferent signals sent along the fibers of the vagus nerve to the pacemaker cells of the heart and the atrial myocardium increases. The frequency and strength of heart contractions decrease, which leads to a decrease in IOC and helps reduce increased blood pressure. Thus, baroreceptors monitor not only changes in blood pressure, their signals are used to reflate pressure when it deviates from the normal level. These receptors and the reflexes they produce are sometimes called “blood pressure regulators.”
Rice. 2. The influence of the sympathetic nervous system on the lumen of arterial vessels muscular type and blood pressure at its low (left) and high (right) tone
A different direction of the reflex reaction occurs in response to a decrease in blood pressure. It is manifested by vasoconstriction and increased heart function, which contribute to an increase in blood pressure.
Reflex vasoconstriction and increased heart function are observed with increased activity of chemoreceptors located in the aortic and carotid bodies. These receptors are already active at normal voltage in the arterial blood, pCO 2 and pO 2. From them there is a constant flow of afferent signals to the neurons of the pressor section of the vasomotor center and to the neurons respiratory center medulla oblongata. The activity of 0 2 receptors increases with a decrease in pO 2 in arterial blood plasma, and the activity of CO 2 receptors increases with an increase in pCO 2 and a decrease in pH. This is accompanied by an increase in the sending of signals to the medulla oblongata, an increase in the activity of neurons in the pressor region and the activity of preganglionic neurons. sympathetic division ANS in the spinal cord, which send higher frequency efferent signals to the blood vessels and heart. The blood vessels narrow, the heart increases the frequency and strength of contractions, which leads to an increase in blood pressure.
The described reflex reactions of blood circulation are called own, since their receptor and effector links belong to the structures of cardio-vascular system. If reflex influences on blood circulation are carried out from a reflexogenic zone located outside the heart and blood vessels, then such reflexes are called conjugated. The Goltz reflex is manifested by the fact that when holding your breath in position take a deep breath and increased pressure in abdominal cavity there is a decrease in heart rate. If such a decrease exceeds 6 contractions per minute, then this indicates increased excitability neurons of the vagus nerve nuclei. Effects on skin receptors can cause both inhibition and activation of cardiac activity. For example, when cold receptors in the skin in the abdominal area are irritated, the heart rate decreases.
During psychoemotional arousal, due to stimulating descending influences, neurons of the pressor section of the vasomotor center are activated, which leads to activation of neurons of the sympathetic nervous system and an increase in blood pressure. A similar reaction develops with ischemia of the central nervous system.
The neuro-reflex effect on blood pressure is achieved by the influence of norepinephrine and adrenaline through stimulation of adrsioreceptors and intracellular mechanisms smooth myocytes of blood vessels and myocytes of the heart.
Centers for circulatory regulation located in the spinal cord, medulla oblongata, hypothalamus and cerebral cortex. Many other structures of the central nervous system can influence blood pressure levels and heart function. These influences are realized primarily through their connections with the centers of the medulla oblongata and spinal cord.
TO spinal cord centers These include preganglionic neurons of the sympathetic division of the ANS (lateral horns of the C8 - L3 segments), which send axons to ganglion neurons located in the prevertebral and paravertebral ganglia and directly innervate vascular smooth myocytes, as well as preganglionic neurons of the lateral horns (Th1-Th3), which regulate the work heart through modulation of the activity of ganglion neurons mainly in the cervical ganglia).
The neurons of the sympathetic nervous system of the lateral horns of the spinal cord are effector neurons. Through them the centers of regulation of blood circulation of the medulla oblongata and more high levels Central nervous system (hypothalamus, raphe nucleus, pons, periaqueductal Gray matter midbrain) affect vascular tone and heart function. At the same time, experimental and clinical observations indicate that these neurons reflexively regulate blood flow in certain areas of the vascular bed, and also independently regulate blood pressure levels when the connection between the spinal cord and the brain is disrupted.
The ability to regulate blood pressure by neurons of the sympathetic nervous system of the spinal cord is based on the fact that their tone is determined not only by the influx of signals from the overlying parts of the central nervous system, but also by the influx of nerve impulses to them from mechano-, chemo-, thermo- and pain receptors of blood vessels, internal organs, skin, musculoskeletal system. When the influx of afferent nerve impulses to these neurons changes, their tone also changes, which is manifested by a reflex narrowing or dilation of blood vessels and an increase or decrease in blood pressure. Such reflex effects on the lumen of blood vessels from the spinal centers of blood circulation regulation provide a relatively rapid reflex increase or restoration of blood pressure after its decrease in conditions of rupture of connections between the spinal cord and the brain.
Located in the medulla oblongata vasomotor center, open F.V. Ovsyannikov. It is part of the cardiovascular, or cardiovascular, center of the central nervous system. In particular, in reticular formation In the medulla oblongata, together with neurons that control vascular tone, neurons of the center for regulating cardiac activity are located. The vasomotor center is represented by two sections: the pressor, the activation of neurons of which causes vasoconstriction and an increase in blood pressure, and the depressor, the activation of neurons of which leads to a decrease in blood pressure.
As can be seen from Fig. 3, neurons of the pressor and depressor regions receive various afferent signals and differently associated with effector neurons. Neurons of the pressor region receive afferent signals along the fibers of the IX and X cranial nerves from vascular chemoreceptors, signals from chemoreceptors of the medulla oblongata, from neurons of the respiratory center, hypothalamic neurons, and also from cortical neurons big brain.
Axons of neurons of the pressor region form excitatory synapses on the bodies of preganglionic sympathetic neurons of the horacolumbar region of the spinal cord. With increased activity, the neurons of the pressor region send an increased flow of efferent nerve impulses to the neurons of the sympathetic region of the spinal cord, increasing their activity and thereby the activity of the ganglion neurons that innervate the heart and blood vessels (Fig. 4).
Rice. 3. Schematic representation of the structure and connections of the centers of reflex regulation of blood circulation (A. Schmidt, 2005)
Preganglonar neurons of the spinal centers, even under resting conditions, have tonic activity and constantly send signals to ganglion neurons, which, in turn, send rare (frequency 1-3 Hz) nerve impulses to the vessels. One of the reasons for the generation of these nerve impulses is the arrival of descending signals to the neurons of the spinal centers from some of the neurons of the pressor department, which have spontaneous, pacemaker-like activity. Thus, the spontaneous activity of neurons of the pressor region, preganglionic spinal centers for circulatory regulation and ganplion neurons are, under resting conditions, a source of tonic activity of sympathetic nerves, which have a vasoconstrictor effect on the vessels.
Rice. 4. Response of baroreceptors, neurons of the cardiovascular center to changes in blood pressure and reflex effects on the work of the heart and the lumen of blood vessels (Schmidt, 2005)
An increase in the activity of preganglionic neurons, caused by an increased influx of signals from the pressor department, has a stimulating effect on the work of the heart, the tone of arterial and venous vessels. In addition, activated neurons of the pressor region are able to inhibit the activity of neurons of the depressor region.
Individual pools of neurons in the pressor region may exert more strong effect to certain areas of the vascular bed. Thus, the excitation of some of them leads to a greater constriction of the vessels of the kidneys, while the excitation of others leads to a significant constriction of the blood vessels gastrointestinal tract and less vasoconstriction skeletal muscles. Inhibition of the activity of neurons in the pressor region leads to a decrease in blood pressure due to the elimination of the vasoconstrictor effect, suppression or loss of the reflex stimulating effect of the sympathetic nervous system on the work of the heart when chemo- and baroreceptors are irritated.
Neurons of the depressor section of the vasomotor center of the medulla oblongata receive afferent signals along the fibers of the IX and X cranial nerves from the baroreceptors of the aorta, blood vessels, heart, as well as from neurons of the hypothalamic center for circulatory regulation, from neurons of the limbic system, and cerebral cortex. When their activity increases, they inhibit the activity of neurons in the pressor region and can, through inhibitory synapses, reduce or eliminate the activity of preganglionic neurons in the sympathetic region of the spinal cord.
There is a reciprocal relationship between the depressor and pressor sections. If, under the influence of afferent signals, the depressor section is excited, this leads to inhibition of the activity of the pressor section and the latter sends a lower frequency of efferent nerve impulses to the neurons of the spinal cord, causing less vasoconstriction. A decrease in the activity of spinal neurons can lead to the cessation of their sending of efferent nerve impulses to the vessels, causing the dilation of blood vessels to the lumen, determined by the level of basal tone of the smooth myocytes of their wall. When blood vessels dilate, blood flow through them increases, the OPS value decreases and blood pressure decreases.
IN hypothalamus There are also groups of neurons, the activation of which causes changes in the functioning of the heart, the reaction of blood vessels and affects blood pressure. These influences can be realized by the hypothalamic centers through changes in the tone of the ANS. Let us recall that an increase in the activity of the neural centers of the anterior hypothalamus is accompanied by an increase in the tone of the parasympathetic division of the ANS, a decrease in the pumping function of the heart and blood pressure. An increase in neural activity in the posterior hypothalamus is accompanied by an increase in the tone of the sympathetic division of the ANS, increased heart function and an increase in blood pressure.
Hypothalamic centers for circulatory regulation are of leading importance in the mechanisms of integration of the functions of the cardiovascular system and other autonomic functions of the body. It is known that the cardiovascular system is one of the most important in the mechanisms of thermoregulation, and its active use in thermoregulation processes is initiated by the hypothalamic centers for regulating body temperature (see “Thermoregulation”). The circulatory system actively responds to changes in blood glucose levels, osmotic pressure blood, to which the neurons of the hypothalamus are highly sensitive. In response to a decrease in blood glucose levels, the tone of the sympathetic nervous system increases, and with an increase in the osmotic pressure of the blood, vosopressin is formed in the hypothalamus, a hormone that has a constricting effect on blood vessels. The hypothalamus influences blood circulation through other hormones, the secretion of which is controlled by the sympathetic division of the ANS (adrenaline, norepinephrine) and hypothalamic liberins and statins (corticosteroids, sex hormones).
Structures of the limbic system, which are part of the emotiogenic areas of the brain, through connections with the hypothalamic centers for circulatory regulation, can have a pronounced effect on the functioning of the heart, vascular tone and blood pressure. An example of such an influence is the well-known increase in heart rate, stroke volume and blood pressure during excitement, dissatisfaction, anger, and emotional reactions of other origins.
Bark cerebral hemispheres also affects the functioning of the heart, vascular tone and blood pressure through connections with the hypothalamus and neurons of the cardiovascular center of the medulla oblongata. The cerebral cortex can influence blood circulation by participating in the regulation of the release of adrenal hormones into the blood. Local irritation of the motor cortex causes an increase in blood flow in the muscles in which contraction is initiated. Reflex mechanisms play an important role. It is known that due to the formation of conditioned vasomotor reflexes, changes in blood circulation can be observed in the pre-start state, even before the onset of muscle contraction, when the pumping function of the heart increases, blood pressure increases and the intensity of blood flow in the muscles increases. Such changes in blood circulation prepare the body to perform physical and emotional stress.
Medium-term response mechanisms Changes in blood pressure begin to act after tens of minutes and hours.
Among the medium-term response mechanisms important role belongs to the mechanisms of the kidney. Thus, with a prolonged decrease in blood pressure and thereby a decrease in blood flow through the kidney, the cells of its juxtaglomsular apparatus react by releasing the enzyme renin into the blood, under the influence of which angiotensin I (AT I) is formed from α 2 - globulin in the blood plasma, and from it, under the influence of the angiotensin-converting enzyme (APF) is formed by AT II. AT II causes contraction of smooth muscle cells in the vascular wall and has a strong vasoconstrictor effect on arteries and veins, increases the return of venous blood to the heart, stroke volume and increases blood pressure. An increase in the level of renin in the blood is also observed with an increase in the tone of the sympathetic section of the ANS and a decrease in the level of Na ions in the blood.
The mechanisms of medium-term response to changes in blood pressure include changes in transcapillary water exchange between blood and tissues. With a prolonged increase in blood pressure, the filtration of water from the blood into the tissues increases. Due to the release of fluid from the vascular bed, the blood volume decreases, which helps to lower blood pressure. Reverse phenomena can develop with a decrease in blood pressure. A consequence of excessive filtration of water into the tissue with an increase in blood pressure may be the development of tissue edema, observed in patients with arterial hypertension.
Medium-term mechanisms for regulating blood pressure include mechanisms associated with the reaction of smooth myocytes of the vascular wall to a long-term increase in blood pressure. With a prolonged increase in blood pressure, vascular stress relaxation is observed - relaxation of smooth myocytes, promoting vasodilation, reducing peripheral resistance to blood flow and reducing blood pressure.
Slow response mechanisms Changes in blood pressure and disruption of its regulation begin to act days and months after its change. The most important of them are the renal mechanisms of blood pressure regulation, realized through changes in blood volume. A change in BCC is achieved through the influence of signaling molecules of the renin-angiotensin H-aldosterone system, natriuretic peptide (NUP) and antidiuretic hormone (ADH) on the processes of filtration and reabsorption of Na+ ions, filtration and reabsorption of water and urine excretion.
With high blood pressure, the excretion of fluid in the urine increases. This leads to a gradual decrease in the amount of fluid in the body, a decrease in bcc, a decrease in venous return of blood to the heart, a decrease in SV, IOC and blood pressure. The main role in the regulation of renal diuresis (volume of urine excreted) is played by ADH, aldoeterone and NUP. With an increase in the content of ADH and aldosterone in the blood, the kidneys increase the retention of water and sodium in the body, contributing to an increase in blood pressure. Under the influence of NUP, the excretion of sodium and water in the urine increases, diuresis increases, and blood volume decreases, which is accompanied by a decrease in blood pressure.
The level of ADH in the blood and its formation in the hypothalamus depend on the BCC. the value of blood pressure, its osmotic pressure and the level of AT II in the blood. Thus, the level of ADH in the blood increases with a decrease in blood volume, a decrease in blood pressure, an increase in blood osmotic pressure, and an increase in the level of AT II in the blood. In addition, the release of ADH into the blood by the pituitary gland is influenced by the influx of afferent nerve impulses from baroreceptors, atrial stretch receptors and large veins into the vasomotor center of the medulla oblongata and the hypothalamus. With an increase in the influx of signals in response to the distension of the atria and large veins by the blood, a decrease in the release of ADH into the blood, a decrease in water reabsorption in the kidneys, an increase in diuresis and a decrease in volume are observed.
The level of aldosterone in the blood is controlled by the action of AT II, ACTH, Na+ and K+ ions on the cells of the glomerular layer of the adrenal glands. Aldoetherone stimulates the synthesis of sodium transport protein and increases sodium reabsorption in the renal tubules. Aldoetherone thereby reduces the excretion of water by the kidneys, promotes an increase in BCC and an increase in blood pressure, an increase in blood pressure by increasing the sensitivity of vascular smooth myocytes to the action of vasoconstrictors (adrenaline, angiotensin).
The main amount of NUP is formed in the atrial myocardium (for which reason it is also called atriopeptide). Its release into the blood increases with increasing atrial stretch, for example, under conditions of increased blood volume and venous return. Natriuretic peptide helps reduce blood pressure by reducing the reabsorption of Na+ ions in the renal tubules, increasing the excretion of Na+ ions and water in the urine and reducing the volume of blood volume. In addition, NUP has a dilating effect on blood vessels, blocking calcium channels smooth myocytes of the vascular wall, reducing the activity of the renin-angiotheisin system and the formation of endothelins. These effects of NUP are accompanied by a decrease in the resistance to blood flow and lead to a decrease in blood pressure.
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 region of the bifurcation of the common 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 (a branch of the glossopharyngeal nerve). From the baroreceptors of the aortic arch, afferent impulses arrive along the vagus nerve. Physiological significance There are more carotid baroreceptors than 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 of1-2 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 fluid to shift from blood vessels in 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.
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.
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;
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, the opposite 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, the content of water and electrolytes in the blood first 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.
Fig.8. Scheme of a functional system for maintaining blood pressure at a level optimal for metabolism.
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