What affects vascular tone, how dangerous are changes in pressure in blood vessels? Humoral regulation of vascular tone Humoral regulation of vascular tone.
Nervous regulation. The main center for the regulation of cardiac activity is located in the medulla oblongata. Excitation of the sympathetic nerves increases the strength of cardiac contractions (positive inotropic effect), frequency (positive chronotropic effect), excitability (positive bathmotropic effect) and conductivity (positive dromotropic effect) of the heart muscle. Trophic or reinforcing nerve I.P. Pavlova (a branch of the sympathetic nerve) has only a positive inotropic effect. The vagus nerve (parasympathetic) has negative ino-, chrono-, batmo- and dromotropic effects on the heart. The heart is under the tone of the vagus nerve (a constant inhibitory effect on the heart).
Hemodynamic mechanisms of regulation: heterometric regulation (Frank-Starling law) - the more the muscle fibers are stretched during diastole, the greater the blood flow to the heart, the greater the force of heart contractions. Homeometric regulation (does not depend on the initial length of muscle fibers) – Bowditch’s “ladder” (an increase in the frequency of heart contractions with a constant strength of the stimulus leads to an increase in the force of heart contractions), Anrep’s phenomenon (the higher the pressure in the aorta and pulmonary artery, the greater the force of heart contractions ).
Reflex regulation of the heart: intracardiac peripheral reflexes (due to the functioning of the intraorgan nervous system: all parts of the reflex arc are located in the heart), extracardiac mechanisms: reflexes from heart to heart (Bainbridge zone), reflexes from vessels to the heart (sinocarotid zone and aortic arch zone ), reflexes from organs to the heart (Goltz and Daninya Aschner reflex).
Humoral regulation of the heart: adrenaline, norepinephrine and dopamine have positive ino-, chrono-, batmo- and dromotropic effects on the heart; acetylcholine - negative foreign, chrono-, batmo- and dromotropic effects; thyroxine – positive chronotropic effect; glucagon – positive ino- and chronotropic effects; corticosteroids and angiotensin – positive inotropic effect. Calcium ions have positive bathmo- and inotropic effects, an overdose causes cardiac arrest in systole; potassium ions (large doses) – negative batmo- and dromotropic effects and cardiac arrest in diastole.
Heart research methods: examination, palpation, percussion, auscultation, determination of systolic and minute blood volumes, electrocardiography, vectorcardiography, phonocardiography, ballistocardiography, echocardiography, etc.
Vascular system. The movement of blood through the vessels is subject to the laws of hemodynamics, which is a branch of hydrodynamics. Functional classification of vessels: shock-absorbing vessels (elastic type vessels); resistive vessels (resistance vessels); sphincter vessels; exchange vessels; capacitive vessels; shunt vessels (arteriovenous anastomoses). Blood circulation parameters: blood pressure; linear blood flow velocity; volumetric blood flow velocity; blood circulation time. Factors determining blood pressure (BP): heart function, resistance and elasticity of the vascular wall, circulating blood mass, blood viscosity, neurohumoral influences. There are systolic, diastolic, pulse and mean arterial pressure. Linear blood flow velocity- the distance that a blood particle travels through vessels of a certain caliber per unit time. Volumetric blood flow velocity- the amount of blood flowing through vessels of a certain caliber per unit of time. Blood circulation rate- the time during which a blood particle passes through the systemic and pulmonary circulation. Arterial pulse- rhythmic oscillations of the artery wall caused by increased pressure during systole. Venous pulse- pulse fluctuations of the wall of a large vein, caused by difficulty in the flow of blood from the veins to the heart during systole of the atria and ventricles.
Microcirculation - processes of blood movement through the smallest blood and lymphatic vessels. Microcirculation includes processes associated with intraorgan blood circulation, which ensures tissue metabolism, redistribution and deposition of blood. In the microcirculation system, there are 2 types of blood flow: slow transcapillary and fast juxtacapillary.
Neurohumoral regulation of vascular tone . Nervous regulation. The main vasomotor center is located in the medulla oblongata. Sympathetic nerves constrict blood vessels; some parasympathetic nerves (glossopharyngeal, lingual, upper laryngeal, pelvic) dilate the vessels of the organ they innervate. The vessels are under constant tone of the sympathetic nerves. Basal tone is due to the vascular wall itself. Additional factors that dilate blood vessels: irritation of the dorsal roots of the spinal cord, axon reflex, irritation of sympathetic cholinergic fibers. Reflex regulation: own reflexes - reflexes from vessels to vessels (sinocarotid and aortic zones) and conjugate reflexes - from organs to vessels. Humoral regulation: vasoconstrictors - adrenaline, norepinephrine, vasopressin, serotonin, renin, endothelin, calcium ions; vasodilators - acetylcholine, histamine, bradykinin, prostaglandins, lactic and pyruvic acids, adenosine, carbon dioxide, nitric oxide, potassium and sodium ions.
Vascular research methods: sphygmography, phlebography, plethysmography, rheography.
The lymphatic system is a drainage system through which tissue fluid flows into the bloodstream (venous system). Lymphatic capillaries are closed. Lymphangion is the area of the lymph vessel between two valves. Lymph nodes are filters that retain microorganisms, tumor cells, and foreign particles; contain T- and B-lymphocytes responsible for immunity; they produce plasma cells that produce antibodies. Functions of the lymphatic system: return proteins, electrolytes and water from the interstitium to the circulatory system; resorptive, barrier, immunobiological, participation in fat metabolism and metabolism of fat-soluble vitamins. Composition of lymph: proteins (albumin, globulins, fibrinogen), lipids, enzymes (lipase and diastase); chlorine and bicarbonates; many lymphocytes, few granulocytes and monocytes.
Lesson 1. Cardiac cycle. Spread of excitation in
heart. Automation. Conduction system of the heart.
Task 1. Cardiac cycle in a frog (Exp. pp. 87-89).
Task 2. Analysis of the cardiac conduction system using the overlay method
ligatures (Stannius ligatures) (Rev. pp. 90-92).
Lesson 2. Properties of the heart muscle. Change in excitability
cardiac muscle in different phases of cardiac
activities. Extrasystole.
Task 1. Reproduction of extrasystole (Ex. p. 98).
Lesson 3. Nervous and humoral regulation of the heart.
Task 1. The influence of irritation of the vago-sympathetic trunk on
activity of the frog's heart. (Exp. pp. 111-113).
Lesson 4. Methods for studying the heart. Electrical phenomena in
heart. Electrocardiography.
Task 1. Registration of an electrocardiogram. (Exp. p. 105).
Task 2. Determination of physical performance (PWC 170 test)
(Exp. p. 436)
Lesson 5. Physiology of blood vessels. Basic laws of hemodynamics.
Task 1. Measuring blood pressure in humans (using the method
Riva-Rochi-Korotkova) (Pr. p. 127).
Task 2. Observation of blood flow in the swimming membrane of the paw
frogs (Ex. p. 136).
Lesson 6. Methods for studying blood flow. Coronary
blood flow
PHYSIOLOGY OF REPEATMENT.
Breath - a complex, cyclically occurring physiological process that ensures gas exchange (O 2 and CO 2) between the environment and the body in accordance with its metabolic needs. The breathing process can be divided into several stages: external respiration (exchange of gases between atmospheric and alveolar air - “pulmonary ventilation”; gas exchange between the blood of the pulmonary capillaries and alveolar air); transport of gases by blood; exchange of gases between blood and body cells; internal or tissue respiration.
External respiration system, includes the lungs and pulmonary circulation (provide arterialization of blood), the chest with respiratory muscles (provide the respiratory act) and the respiratory regulation system (respiratory center and other parts of the central nervous system). Inhale: impulse from the respiratory center - contraction of inspiratory respiratory muscles (diaphragm and external intercostal muscles during quiet inspiration) - increase in chest volume - increase in negative pressure in the pleural cavity - increase in lung volume - decrease in intrapulmonary pressure below atmospheric pressure - entry of air into the lungs. Negative pressure in the pleural cavity caused by elastic traction of the lungs. Elastic traction of the lungs-the force with which the lungs constantly strive to reduce their volume.
Pneumothorax- entry of air into the pleural cavity. Atelectasis- collapse of the alveoli.
Lung volumes and capacities: vital capacity (VC), which includes tidal volume (TI), inspiratory reserve volume (IRV) and expiratory reserve volume (ERV); residual volume (VR); functional residual capacity (FRC=ROvyd+OO); total lung capacity VC+OO); the volume of dead space (air located in the airways and not participating in gas exchange) included in the sediment. Pulmonary ventilation. Minute volume of respiration (MOD = DO x RR). Alveolar ventilation = (DO-volume of dead space) x RR. Gas exchange indicators: oxygen consumption (VO 2), oxygen utilization factor (KIO 2).
Transport of gases by blood. The mechanism of transfer of oxygen from the alveolar air to the blood and carbon dioxide from the blood to the alveolar air is diffusion. Forms of oxygen transfer: oxygen dissolved in plasma; in the form of oxyhemoglobin. Blood oxygen capacity- the maximum amount of oxygen that hemoglobin can bind when it is completely saturated with oxygen. The oxyhemoglobin dissociation curve is the dependence of the binding of oxygen in the blood on its partial pressure. Factors influencing its shifts to the right and left (pCO2, temperature, pH). Forms of carbon dioxide transfer: carbon dioxide dissolved in plasma; in the form of carbhemoglobin; in the form of sodium bicarbonates (in plasma) and potassium (in erythrocytes).
Neurohumoral regulation of breathing. Nervous regulation. Centers: spinal (C3-C5 and T2-T10); bulbar (main), consisting of inspiratory and expiratory sections, possessing automaticity; pons (pneumotaxic). The phrenic nerve and intercostal nerves innervate the respiratory muscles. Reflex regulation - respiratory reflexes begin with various receptors: slowly adapting lung stretch receptors (Hering-Breuer reflex, vagus nerve), irritant rapidly adapting mechanoreceptors (cough, bronchospasm), J-receptors, or " juxtacapillary receptors of the lungs (pulmonary edema), proprioceptors of the respiratory muscles, peripheral (arterial in the carotid sinuses) and central (in the hypothalamus) chemoreceptors. Humoral regulation: Hypercapnia (increased CO2 in the blood), hypoxia (lack of oxygen in tissues) and hydrogen ions (acidosis) stimulate respiration. Hypocapnia (decrease in CO2 in the blood) and hyperoxia (increase in O2 in the alveolar air) depress respiration. Frederick's experience with cross-circulation. Haldane's experiment.
Methods for studying respiratory function: spirometry and spirography, pneumotachography.
Lesson 1. External breathing. Lung volumes and capacities.
Task 1. Spirometry: dry and water spirometers (Ref. page 174).
Task 2. Determination of minute volume of breathing at rest and during
physical activity (Ex. p. 188).
Lesson 2. Gas exchange in the lungs. Transport of gases by blood.
Task 1. Gas analysis of atmospheric, exhaled, alveolar air
using gas analyzers. (Demonstration).
Task 2. Determination of pH, pO 2, pCO 2 in arterialized blood with
using a microanalyzer. (Demonstration).
Lesson 3. Regulation of breathing.
Task 1. Pneumography (Pr. p. 182).
Task 2. Assessing the patency of the tracheobronchial tree using
device "Pneumoscreen-2". (Demonstration).
Related information.
Vascular tone- this is a certain constant tension of the vascular walls that determines the lumen of the vessel.
Regulation vascular tone is carried out local And systemic nervous and humoral mechanisms.
Thanks to automation some smooth muscle cells of vessel walls, blood vessels, even in the conditions of their denervation, have original(basal )tone , which is characterized self-regulation.
Thus, with an increase in the degree of stretching of smooth muscle cells basal tone increases(especially pronounced in arterioles).
Layers on the basal tone tone, which is provided by nervous and humoral regulation mechanisms.
The main role belongs to the nervous mechanisms that reflexively regulate lumen of blood vessels.
Strengthens basal tone constant tone of the sympathetic centers.
Nervous regulation carried out vasomotors, i.e. nerve fibers that end in muscle vessels (with the exception of exchange capillaries, where there are no muscle cells). IN gas engines refer to autonomic nervous system and are divided into vasoconstrictors(vasoconstriction) and vasodilators(expand).
Most often, sympathetic nerves are vasoconstrictors, since their transection is accompanied by vasodilation.
Sympathetic vasoconstriction is considered a systemic mechanism for regulating the lumen of blood vessels, because it is accompanied by an increase in blood pressure.
The vasoconstrictor effect does not extend to the vessels of the brain, lungs, heart and working muscles.
When the sympathetic nerves are excited, the vessels of these organs and tissues dilate.
TO vasoconstrictors include:
1. Sympathetic adrenergic nerve fibers innervating the vessels of the skin, abdominal organs, parts of skeletal muscles (when interacting norepinephrine with a- adrenergic receptors). Their centers located in all thoracic and three upper lumbar segments of the spinal cord.
2. Parasympathetic cholinergic nerve fibers going to the vessels of the heart. Vasodilator nerves are often part of the parasympathetic nerves. However, vasodilator nerve fibers are also found in the sympathetic nerves, as well as in the dorsal roots of the spinal cord.
TO vasodilators (there are fewer of them than vasoconstrictors) include:
1. Adrenergic sympathetic nerve fibers innervating blood vessels.
Parts of skeletal muscles (when interacting norepinephrine with b- adrenoreceptors);
Hearts (when interacting norepinephrine with b 1 - adrenoreceptors).
2. Cholinergic sympathetic nerve fibers that innervate the vessels of some skeletal muscles.
3. Cholinergic parasympathetic fibers of the vessels of the salivary glands (submandibular, sublingual, parotid), tongue, gonads.
4. Metasympathetic nerve fibers, innervating the vessels of the genital organs.
5. Histaminergic nerve fibers (related to regional or local regulatory mechanisms).
Vasomotor center is a set of structures at various levels of the central nervous system that provide regulation of blood supply.
Humoral regulation vascular tone is carried out by biologically active substances and metabolic products. Some substances dilate, others constrict blood vessels, some have a dual effect.
1. Vasoconstrictors are produced in various cells of the body, but more often in transducer cells (similar to chromaffin cells of the adrenal medulla). The most powerful substance that narrows arteries, arterioles and, to a lesser extent, veins is angiotensin, produced in the liver. However, in blood plasma it is in an inactive state. It is activated by renin (renin-angiotensin system).
As blood pressure decreases, renin production in the kidney increases. Renin by itself does not constrict blood vessels; being a proteolytic enzyme, it breaks down plasma α2-globulin (angiotensinogen) and converts it into a relatively inactive decapeptide (angiotensin I). The latter, under the influence of angiotensinase, an enzyme fixed on the cell membranes of the capillary endothelium, is converted into angiotensin II, which has a strong vasoconstrictor effect, including on the coronary arteries (the mechanism of activation of angiotensin is similar to membrane digestion). Angiotensin also provides vasoconstriction by activating the sympathetic-adrenal system. Vasoconstrictor effect of angiotensin-
on II, its strength exceeds the influence of nor-adrenaline by more than 50 times. With a significant increase in blood pressure, renin is produced in smaller quantities, blood pressure decreases and returns to normal. Angiotensin does not accumulate in large quantities in the blood plasma, as it is quickly destroyed in the capillaries by angiotensinase. However, in some kidney diseases, as a result of which their blood supply deteriorates, even with normal initial systemic blood pressure, the amount of released renin increases and develops hypertension renal origin.
Vasopressin(ADH is an antidiuretic hormone) also constricts blood vessels, its effects are more pronounced at the level of arterioles. However, vasoconstrictive effects are only well manifested with a significant drop in blood pressure. In this case, a large amount of vasopressin is released from the posterior lobe of the pituitary gland. When exogenous vasopressin is introduced into the body, vasoconstriction is observed, regardless of the initial level of blood pressure. Under normal physiological conditions, its vasoconstrictor effect is not manifested.
Norepinephrine acts mainly on α-adrenergic receptors and constricts blood vessels, as a result of which peripheral resistance increases, but the effects are small, since the endogenous concentration of norepinephrine is low. With exogenous administration of norepinephrine, blood pressure increases, as a result of which reflex bradycardia occurs, cardiac function decreases, which inhibits the pressor effect.
Vasomotor center. Levels of central regulation of vascular tone (spinal, bulbar, hypothalomic cortical). Features of reflex and humoral regulation in the circulatory system in children
Vasomotor center - a set of neurons located at various levels of the central nervous system and regulating vascular tone.
The CNS contains next levels
:
spinal;
bulbar;
hypothalamic;
cortical.
2. The role of the spinal cord in the regulation of vascular tone Spinal cord plays a role in the regulation of vascular tone.
Neurons that regulate vascular tone: nuclei of sympathetic and parasympathetic nerves innervating blood vessels. The spinal level of the vasomotor center was discovered in 1870. Ovsyannikov. He cut the central nervous system at various levels and found that in a spinal animal, after removal of the brain, the blood pressure (BP) decreases, but then gradually recovers, although not to the original level, and is maintained at a constant level.
The spinal level of the vasomotor center does not have much independent significance; it transmits impulses from the overlying parts of the vasomotor center.
3. The role of the medulla oblongata in the regulation of vascular tone Medulla oblongata also plays a role in the regulation of vascular tone.
Bulbar section of the vasomotor center opened: Ovsyannikov and Ditegar(1871-1872). In a bulbar animal, the pressure remains almost unchanged, i.e. The main center that regulates vascular tone is located in the medulla oblongata.
Ranson and Alexander. Point irritation of the medulla oblongata revealed that in the bulbar part of the vasomotor center there are pressor and depressor zones. The pressor zone is in the rostral region, the depressor zone is in the caudal region.
Sergievsky, Valdian. Modern views: the bulbar section of the vasomotor center is located at the level of neurons of the reticular formation of the medulla oblongata. The bulbar section of the vasomotor center contains pressor and depressor neurons. They are located diffusely, but in the rostral region there are more pressor neurons, and in the caudal region there are more depressor neurons. The bulbar section of the vasomotor center contains cardioinhibitory neurons. There are more pressor neurons than depressor neurons. That. when the vasomotor center is excited, a vasoconstrictor effect occurs.
There are 2 zones in the bulbar section of the vasomotor center: lateral and medial
.
Lateral zone consists of small neurons that mainly perform an afferent function: they receive impulses from receptors of the heart vessels, internal organs, and exteroceptors. They do not cause a response, but transmit impulses to the neurons of the medial zone.
Medial zone consists of large neurons that perform an efferent function. They do not have direct contacts with receptors, but receive impulses from the lateral zone and transmit impulses to the spinal vasomotor center.
4. Hypothalamic level of regulation of vascular tone Consider the hypothalamic level of the vasomotor center.
When the anterior groups of hypothalamic nuclei are excited, the parasympathetic nervous system is activated - a decrease in tone. Irritation of the posterior nuclei produces mainly a vasoconstrictor effect.
Features of hypothalamic regulation:
carried out as a component of thermoregulation;
the lumen of blood vessels changes in accordance with changes in the temperature of the environment.
The hypothalamic section of the vasomotor center ensures the use of skin coloring in emotional reactions. The hypothalamic section of the vasomotor center is closely connected with the bulbar and cortical sections of the vasomotor center.
5. Cortical section of the vasomotor center Methods for studying the role of the cortical part of the vasomotor center.
Irritation method: It was discovered that irritated parts of the cerebral cortex, when excited, change vascular tone. The effect depends on the strength and is most pronounced when irritating the anterior central gyrus, frontal and temporal zones of the cerebral cortex.
Conditioned reflex method: it was discovered that the cerebral cortex ensures the development of conditioned reflexes for both dilation and constriction of blood vessels.
Metronome > adrenaline > skin vasoconstriction.
Metronome > saline > cutaneous vasoconstriction.
Conditioned reflexes are developed faster for contraction than for expansion. Due to the cortical part of the vasomotor center, the vascular response adapts to changes in environmental conditions.
In childhood, the functional state of nerve cells is very variable: the level of their excitability changes, and strong or prolonged excitation easily turns into inhibition. This feature of nerve cells explains the instability of the heartbeat rhythm characteristic of children of early and preschool age. An electrocardiogram, i.e. a graphic recording of heart impulses, using electrical sensors shows that heartbeat cycles differ markedly from each other in their duration and height teeth and the duration of the intervals between individual teeth. Reflex changes in the functioning of the heart and blood vessels, in particular the own reflexes of the circulatory system, aimed at maintaining normal blood pressure, are also unstable.
In subsequent years, the stability of both the rhythm of heart contractions and reflex changes in the heart and blood vessels gradually increases. However, for a long time, often up to 15-17 years, increased excitability of the cardiovascular nerve centers persists. This explains the excessive expression of vasomotor and cardiac reflexes in children. They manifest themselves in paleness or, conversely, redness of the skin of the face, a sinking heart or an increase in its contractions.
This regulation is ensured by a complex mechanism, including sensitive (afferent), central And efferent links.
5.2.1. Sensitive link. Vascular receptors - angioceptors- according to their function they are divided into baroreceptors(pressoreceptors) that respond to changes in blood pressure, and chemoreceptors, sensitive to changes in the chemical composition of the blood. Their largest concentrations are in main reflexogenic zones: aortic, sinocarotid, in the vessels of the pulmonary circulation.
An irritant baroreceptors It is not the pressure as such, but the speed and degree of stretching of the vessel wall by pulse or increasing fluctuations in blood pressure.
Chemoreceptors react to changes in the concentration in the blood of O 2, CO 2, H +, and some inorganic and organic substances.
Reflexes that arise from the receptive zones of the cardiovascular system and determine the regulation of relationships within this particular system are called own (systemic) blood circulation reflexes. When the strength of stimulation increases, in addition to the cardiovascular system, the response involves breath. It will already be conjugate reflex. The existence of conjugate reflexes makes it possible for the circulatory system to quickly and adequately adapt to the changing conditions of the internal environment of the body.
5.2.2. Central link usually called vasomotor (vasomotor) center. Structures related to the vasomotor center are localized in the spinal cord, medulla oblongata, hypothalamus, and cerebral cortex.
Spinal level of regulation. Nerve cells, the axons of which form vasoconstrictor fibers, are located in the lateral horns of the thoracic and first lumbar segments of the spinal cord and are the nuclei of the sympathetic and parasympathetic system.
Bulbar level of regulation. The vasomotor center of the medulla oblongata is the main center for maintaining vascular tone and reflex regulation of blood pressure.
The vasomotor center is divided into depressor, pressor and cardioinhibitory zones. This division is quite arbitrary, since due to the mutual overlap of the zones it is impossible to determine the boundaries.
Depressor zone helps lower blood pressure by reducing the activity of sympathetic vasoconstrictor fibers, thereby causing vasodilation and a drop in peripheral resistance, as well as by weakening sympathetic stimulation of the heart, i.e., reducing cardiac output.
Pressor zone has the exact opposite effect, increasing blood pressure through an increase in peripheral vascular resistance and cardiac output. The interaction of depressor and pressor structures of the vasomotor center is of a complex synergistic-antagonistic nature.
Cardioinhibitory the action of the third zone is mediated by the fibers of the vagus nerve going to the heart. Its activity leads to a decrease in cardiac output and thereby combines with the activity of the depressor zone in reducing blood pressure.
The state of tonic excitation of the vasomotor center and, accordingly, the level of total blood pressure are regulated by impulses coming from the vascular reflexogenic zones. In addition, this center is part of the reticular formation of the medulla oblongata, from where it also receives numerous collateral excitations from all specifically conducting pathways.
Hypothalamic level of regulation plays an important role in the implementation of adaptive circulatory reactions. The integrative centers of the hypothalamus exert a descending influence on the cardiovascular center of the medulla oblongata, ensuring its control. In the hypothalamus, as well as in the boulevard vasomotor center, there are depressor And pressor zones.
Cortical level of regulationn most thoroughly studied using conditioned reflex methods. Thus, it is relatively easy to develop a vascular reaction to a previously indifferent stimulus, causing sensations of heat, cold, pain, etc.
Certain areas of the cerebral cortex, like the hypothalamus, have a descending influence on the main center of the medulla oblongata. These influences are formed as a result of the comparison of information that entered the higher parts of the nervous system from various receptive zones with the previous experience of the body. They ensure the implementation of the cardiovascular component of emotions, motivations, and behavioral reactions.
5.2.3. Efferent link. Efferent regulation of blood circulation is realized through the smooth muscle elements of the blood vessel wall, which are constantly in a state of moderate tension - vascular tone. There are three mechanisms for regulating vascular tone:
1. autoregulation
2. neural regulation
3. humoral regulation
Autoregulation ensures a change in the tone of smooth muscle cells under the influence of local excitation. Myogenic regulation is associated with changes in the state of vascular smooth muscle cells depending on the degree of their stretching - the Ostroumov-Beilis effect. Smooth muscle cells in the vascular wall respond by contracting to stretch and relaxing to lower pressure in the vessels. Meaning: maintaining a constant level of blood volume entering the organ (the most pronounced mechanism is in the kidneys, liver, lungs, and brain).
Nervous regulation vascular tone is carried out by the autonomic nervous system, which has a vasoconstrictor and vasodilator effect.
Sympathetic nerves are vasoconstrictors(constrict blood vessels) for blood vessels of the skin, mucous membranes, gastrointestinal tract and vasodilators(dilate blood vessels) for the vessels of the brain, lungs, heart and working muscles. Parasympathetic the nervous system has a dilating effect on blood vessels.
Almost all vessels are subject to innervation, with the exception of capillaries. The innervation of veins corresponds to the innervation of arteries, although in general the density of innervation of veins is much less.
Humoral regulation carried out by substances of systemic and local action. Systemic substances include calcium, potassium, sodium ions, hormones:
Calcium ions cause vasoconstriction, potassium ions have an expanding effect.
Biologically active substances and local hormones, such as histamine, serotonin, bradykinin, prostaglandins.
Vasopressin– increases the tone of smooth muscle cells of arterioles, causing vasoconstriction;
Adrenalin it affects the arteries and arterioles of the skin, digestive organs, kidneys and lungs vasoconstrictor effect; on the vessels of skeletal muscles, smooth muscles of the bronchi - expanding, thereby promoting the redistribution of blood in the body. During physical stress and emotional arousal, it helps to increase blood flow through skeletal muscles, brain, and heart. The effect of adrenaline and norepinephrine on the vascular wall is determined by the existence of different types of adrenergic receptors - α and β, which are areas of smooth muscle cells with special chemical sensitivity. Vessels usually contain both types of receptors. The interaction of mediators with the α-adrenergic receptor leads to contraction of the vessel wall, and with the β-receptor - to relaxation.
Atrial natriuretic peptide - m powerful vasodilator (dilates blood vessels, lowering blood pressure). Reduces reabsorption (reabsorption) of sodium and water in the kidneys (reduces the volume of water in the vascular bed). It is released by endocrine cells of the atria when they are overstretched.
Thyroxine– stimulates energy processes and causes constriction of blood vessels;
Aldosterone produced in the adrenal cortex. Aldosterone has an unusually high ability to enhance the reabsorption of sodium in the kidneys, salivary glands, and digestive system, thus changing the sensitivity of the vascular walls to the influence of adrenaline and norepinephrine.
Vasopressin causes narrowing of the arteries and arterioles of the abdominal organs and lungs. However, as under the influence of adrenaline, the vessels of the brain and heart respond to this hormone by dilating, which helps to improve the nutrition of both brain tissue and heart muscle.
Angiotensin II is a product of enzymatic breakdown angiotensinogen or angiotensin I under the influence renina. It has a powerful vasoconstrictor (vasoconstrictor) effect, significantly superior in strength to norepinephrine, but unlike the latter, it does not cause the release of blood from the depot. Renin and angiotensin are renin-angiotensin system.
In nervous and endocrine regulation, hemodynamic mechanisms of short-term action, intermediate and long-term action are distinguished. To the mechanisms short-term actions include circulatory reactions of nervous origin - baroreceptor, chemoreceptor, reflex to CNS ischemia. Their development occurs within a few seconds. Intermediate(in time) mechanisms include changes in transcapillary exchange, relaxation of a tense vessel wall, and the reaction of the renin-angiotensin system. It takes minutes for these mechanisms to turn on, and hours for maximum development. Regulatory Mechanisms long-term actions affect the relationship between intravascular blood volume I capacity of vessels. This is accomplished through transcapillary fluid exchange. This process involves renal fluid volume regulation, vasopressin and aldosterone.
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Vascular tone – This is a long-term excitation of the smooth muscle layer of the vascular wall, providing a certain diameter of the vessels and resistance of the vascular wall to blood pressure. Vascular tone is provided by several mechanisms: myogenic, humoral and neuro-reflex.
Myogenic mechanisms of muscle tone provide the so-called basal vascular tone. Basal vascular tone is the part of vascular tone that remains in the vessels in the absence of nervous and humoral influences on them. This component depends only on the properties of the smooth muscle cells that form the basis of the muscular lining of the blood vessels. A characteristic feature of the biological membranes of smooth muscle cells that make up the vascular wall is the high activity of Ca ++ -dependent channels. The activity of these channels ensures a high concentration of Ca ++ ions in the cytoplasm of cells and long-term interaction, in this regard, of actin and myosin.
Humoral mechanisms regulating vascular tone
Humoral influences on the vascular walls are provided by biologically active substances, electrolytes and metabolites.
Effect of biologically active substances on the vascular wall. The group of biologically active substances includes adrenaline, vasopressin, histamine, angiotensin (α 2 - globulin), prostaglandins, bradykinin. Adrenaline can lead to both vasoconstriction and dilation. The effect of the influence depends on the type of receptors with which the adrenaline molecule interacts. If adrenaline interacts with the α-adrenergic receptor, vasoconstriction (vasoconstriction) is observed, but if it interacts with the β-adrenergic receptor, vasodilation (vasodilation) is observed. Atriopeptide, produced in the right side of the heart, causes vasodilation. Vasopressin and angiotensin cause vasoconstriction, histamine, bradykinin, prostaglandins cause vasodilation.
The effect of certain electrolytes on the vascular wall. An increase in the content of Ca++ ions in the vascular wall leads to an increase in vascular tone, and K+ ions to a decrease.
Effect of metabolic products on the vascular wall. The group of metabolites includes organic acids (carbonic, pyruvic, lactic), ATP breakdown products, and nitric oxide. Metabolic products, as a rule, cause a decrease in vascular tone, leading to their expansion.
Neuro-reflex mechanisms of regulation of vascular lumen
Vascular reflexes are divided into congenital (unconditioned, specific) and acquired (conditioned, individual). Congenital vascular reflexes consist of five elements: receptors, afferent nerve, nerve center, efferent nerve and executive organ.
Receptor part of vascular reflexes.
The receptor part of vascular reflexes is represented by baroreceptors, which are located in the walls of blood vessels. However, most of the baroreceptors are concentrated in the reflexogenic zones, which we have talked about several times. We are talking about a paired reflexogenic zone located in the bifurcation zone of the common carotid artery, aortic arch, and pulmonary artery. Volume receptors of the heart, located mainly in the right heart, also take part in the regulation of the lumen of blood vessels. There are several groups of baroreceptors:
baroreceptors that respond to a constant component of blood pressure;
baroreceptors, which respond to rapid, dynamic changes in blood pressure;
baroreceptors that respond to vibrations of the vascular wall.
All other things being equal, receptor activity is higher for rapid changes in blood pressure than for slow changes. In addition, the increase in baroreceptor activity depends on the initial level of blood pressure. So, with an increase in blood pressure by 10 mmHg. from the initial level of 140 mmHg. in the afferent neuron associated with baroreceptors, nerve impulses are noted with a frequency of 5 impulses/sec. With the same increase in blood pressure by 10 mmHg, but from the initial level of 180 mmHg, nerve impulses with a frequency of 25 impulses/sec are noted in the afferent neuron associated with baroreceptors. When high blood pressure values are fixed at one value for a long time, the receptors can adapt to the action of this stimulus and they reduce their activity. In this situation, the nerve centers begin to perceive high blood pressure as normal.
In addition to the nervous regulation of vascular tone, controlled by the sympathetic nervous system, in the human body there is a second way of regulating these same vessels - humoral (liquid), which is controlled by the chemicals of the blood itself flowing in the vessels.
“Regulation of the lumen of blood vessels and blood supply to organs is carried out by reflex and humoral pathways.
...Humoral regulation of vascular tone. Humoral regulation is carried out by chemicals (hormones, metabolic products and others) circulating in the blood or formed in tissues during irritation. These biologically active substances either constrict or dilate blood vessels.” (A.V. Loginov, 1983).
This is a direct clue for searching for the causes of increased blood pressure in pathologies of humoral regulation of vascular tone. It is necessary to study biologically active substances that either constrict (they may do this excessively) or dilate (they may not do this actively enough) blood vessels.
However, if the question was only the study of pathological deviations in the humoral regulation of vascular tone and the study of their effect on blood pressure, then we could immediately stop these studies of ours and declare that in general no real deviations in vascular tone are practically to blame for the increase in maximum blood pressure and the development of hypertension. We already know this for sure!
But biologically active substances in the blood have long been mistakenly considered in medicine to be the culprits of hypertension. This erroneous statement is persistently promoted, so you need to be patient and carefully examine all the biologically active substances in the blood that dilate and constrict blood vessels.
Let's start with a preliminary brief review of these substances, with the accumulation of basic information about them.
Vasoconstrictor chemicals in the blood include: adrenaline, norepinephrine, vasopressin, angiotensin II, serotonin.
Adrenaline is a hormone that is produced in the adrenal medulla. Norepinephrine is a mediator, a transmitter of excitation in adrenergic synapses, secreted by the endings of postganglionic sympathetic fibers. It is also formed in the adrenal medulla.
Adrenaline and norepinephrine (catecholamines) “cause an effect of the same nature as that which occurs when the sympathetic nervous system is excited, that is, they have sympathomimetic (similar to sympathetic) properties. Their content in the blood is negligible, but their activity is extremely high.
...The importance of catecholamines stems from their ability to quickly and intensively influence metabolic processes, increase the performance of the heart and skeletal muscles, ensure the redistribution of blood for optimal supply of tissues with energy resources, and enhance the excitation of the central nervous system.”
(G.N. Kassil. “The internal environment of the body.” 1983).
An increase in the flow of adrenaline and norepinephrine into the blood is associated with stress (including stress reactions as part of diseases) and physical activity.
Adrenaline and norepinephrine cause vasoconstriction of the skin, abdominal organs, and lungs.
In small doses, adrenaline dilates the blood vessels of the heart, brain and working skeletal muscles, increases the tone of the heart muscle, and increases heart rate.
An increase in the flow of adrenaline and norepinephrine into the blood during stress and physical activity ensures an increase in blood flow in the muscles, heart, and brain.
“Of all the hormones, adrenaline has the most dramatic vascular effect. It has a vasoconstrictor effect on the arteries and arterioles of the skin, digestive organs, kidneys and lungs; on the vessels of skeletal muscles, smooth muscles of the bronchi - dilating, thereby promoting the redistribution of blood in the body.
...The influence of adrenaline and norepinephrine on the vascular wall is determined by the existence of different types of adrenergic receptors - which are areas of smooth muscle cells with special chemical sensitivity. The vessels usually contain both types of these α-adrenergic receptors and receptors. The interaction of the mediator with the -receptor leads to relaxation. Norepinephrineb contracts the vessel wall, with - and a-adrenergic receptors, adrenaline - with a interacts mainly with - receptors. According to W. Cannon, adrenaline is an “emergency hormone” that mobilizes the functions and forces of the body in difficult, sometimes extreme conditions.
...The intestine also contains both types of adrenergic receptors; however, exposure to both causes inhibition of smooth muscle activity.
Adrenergic receptors, and herea... There are no adrenergic receptors in the heart and bronchi, which leads to norepinephrine and adrenaline only excite increased heart contractions and dilation of the bronchi.
...Aldosterone is another necessary link in the regulation of blood circulation by the adrenal glands. It is produced in their cortex. Aldosterone has an unusually high ability to enhance the reabsorption of sodium in the kidneys, salivary glands, and digestive system, thus changing the sensitivity of the vascular walls to the influence of adrenaline and norepinephrine.”
Vasopressin (antidiuretic hormone) is secreted into the blood by the posterior pituitary gland. It causes a constriction of arterioles and capillaries of all organs and is involved in the regulation of diuresis (according to A.V. Loginov, 1983). According to A. D. Nozdrachev et al. (1991): Vasopressin “causes a narrowing of the arteries and arterioles of the abdominal organs and lungs. However, as under the influence of adrenaline, the vessels of the brain and heart respond to this hormone by dilating, which improves the nutrition of both brain tissue and heart muscle.”
Angiotensin II. In the kidneys, in their so-called juxtaglomerular apparatus (complex), the proteolytic enzyme renin is produced. In turn, serum β-globulin angiotensinogen is formed in the liver. Renin enters the blood and (plasma) catalyzes the process of converting angiotensinogen into the inactive decapeptide (10 amino acids) angiotensin I. The enzyme peptidase, localized in membranes, catalyzes the cleavage of the dipeptide (2 amino acids) from angiotensin I and converts it into the biologically active octapeitide (8 amino acids) angiotheisin II, which increases blood pressure as a result of narrowing of blood vessels (according to the Encyclopedic Dictionary of Medical Terms, 1982–1984).
Angiotensin II has a powerful vasoconstrictor (vasoconstrictor) effect, significantly superior to norepinephrine. It is very important that angiotensin II, unlike norepinephrine, “does not cause the release of blood from the depot. This is explained by the presence of angiotensin-sensitive receptors only in precapillary arterioles. which are distributed unevenly in the body. Therefore, its effect on the vessels of different areas is not the same. The systemic pressor effect is accompanied by a decrease in blood flow in the kidneys, intestines and skin and an increase in the brain, heart and adrenal glands. Changes in blood flow in the muscle are minor. Large doses of angiotensin can cause constriction of blood vessels in the heart and brain. It is believed that renin and angiotensin constitute the so-called renin-angiotensin system.”
(A.D. Nozdrachev et al., 1991).
Serotonin, discovered in the mid-20th century, by its very name means a substance from blood serum that can increase blood pressure. Serotonin is produced mainly in the intestinal mucosa. It is released by blood platelets and, due to its vasoconstrictive effect, helps stop bleeding.
We got acquainted with the vasoconstrictor substances of the blood. Now let's look at the vasodilatory chemicals in the blood. These include acetylcholine, histamine, bradykinin, prostaglandins.
Acetylcholine is formed in the endings of parasympathetic nerves. It dilates peripheral blood vessels, slows heart contractions, and lowers blood pressure. Acetylcholine is not stable and is extremely quickly destroyed by the enzyme acetylcholinesterase. Therefore, it is generally accepted that the action of acetylcholine in the body is local, limited to the area where it is formed.
“But now... it has been established that acetylcholine enters the blood from organs and tissues and takes an active part in the humoral regulation of functions. Its effect on cells is similar to that of the parasympathetic nerves.”
(G.N. Kassil. 1983).
Histamine is formed in many organs and tissues (liver, kidneys, pancreas and especially in the intestines). It is constantly contained mainly in mast cells of connective tissue and basophilic granulocytes (leukocytes) of the blood.
Histamine dilates blood vessels, including capillaries, increases the permeability of capillary walls with the formation of edema, and causes increased secretion of gastric juice. The action of histamine explains the reaction of redness of the skin. With significant histamine formation, a drop in blood pressure may occur due to the accumulation of a large amount of blood in dilated capillaries. As a rule, allergic phenomena do not occur without the participation of histamine (histamine is released from basophilic granulocytes).
Bradykinin is formed in the blood plasma, but it is especially abundant in the submandibular and pancreas. Being an active polypeptide, it dilates the blood vessels of the skin, skeletal muscles, brain and coronary vessels, leading to a decrease in blood pressure.
“Prostaglandins represent a large group of biologically active substances. They are derivatives of unsaturated fatty acids. Prostaglandins are produced in virtually all organs and tissues, but the term for them is associated with the prostate gland, from which they were first isolated. The biological effects of prostaglandins are extremely diverse. One of their effects is manifested in a pronounced effect on the tone of vascular smooth muscles, and the influence of different types of prostaglandins is often diametrically opposed. Some prostaglandins contract the walls of blood vessels and increase blood pressure, while others have a vasodilatory effect, accompanied by a hypotensive effect.”
(A.D. Nozdrachev et al., 1991).
When studying the influence of biologically active substances in the blood, it is necessary to take into account that in the body there are so-called blood depots, which are also the depot of some of the substances being studied.
A. V. Loginov (1983):
“Blood depot. At rest in humans, up to 40-80% of the total blood mass is located in blood depots: the spleen, liver, subcutaneous choroid plexus and lungs. The spleen contains about 500 ml of blood, which can be completely shut off from circulation. The blood in the vessels of the liver and choroid plexus of the skin circulates 10-20 times slower than in other vessels. Therefore, blood is retained in these organs and they act as blood reserves.
The blood depot regulates the amount of circulating blood. If it is necessary to increase the volume of circulating blood, the latter enters the bloodstream from the spleen due to its contraction. Such a reduction occurs reflexively in cases where the blood becomes depleted of oxygen, for example, during blood loss, low atmospheric pressure, carbon monoxide poisoning, during intense muscular work and in other similar cases. The flow of blood in a relatively increased amount from the liver into the bloodstream occurs due to the more accelerated movement of blood in it, which is also carried out by reflex.”
A. D. Nozdrachev et al (1991):
“Blood depots. In mammals, up to 20% of the total amount of blood can stagnate in the spleen, that is, it can be turned off from the general circulation.
...Thicker blood accumulates in the sinuses, containing up to 20% of the red blood cells of the body’s total blood, which has a certain biological significance.
...The liver is also capable of depositing and concentrating significant amounts of blood without excluding it, unlike the spleen, from the general bloodstream. The deposition mechanism is based on contraction of the diffuse sphincter of the hepatic veins and sinuses with changing blood flow or due to increased blood flow with unchanged outflow. Emptying the depot is carried out reflexively. Adrenaline influences the rapid release of blood. It causes narrowing of the mesenteric arteries and, accordingly, a decrease in blood flow to the liver. At the same time, it relaxes the sphincter muscles and contracts the walls of the sinuses. The release of blood from the liver depends on pressure fluctuations in the vena cava system and the abdominal cavity. This is also facilitated by the intensity of breathing movements and contraction of the abdominal muscles.”
Due to the fact that we are investigating possible regulatory influences that increase blood pressure, it is necessary to take into account an important general point about the time of action of regulatory mechanisms:
“In nervous and endocrine regulation, hemodynamic mechanisms of short-term action, intermediate and long action are distinguished.
Mechanisms of short-term action include circulatory reactions of nervous origin - baroreceptor, chemoreceptor, reflex to CNS ischemia. Their development occurs within a few seconds. Intermediate (in time) mechanisms include changes in transcapillary exchange, relaxation of a tense vessel wall, and the reaction of the renin-angiotensin system. It takes minutes for these mechanisms to turn on, and hours for maximum development. Long-term regulatory mechanisms influence the relationship between intravascular blood volume and vascular capacity. This is accomplished through transcapillary fluid exchange. This process involves renal fluid volume regulation, vasopressin and aldosterone.”
(A.D. Nozdrachev et al., 1991).
We can assume that we have accumulated the necessary basic information for studying the humoral regulation of vascular tone and blood pressure. It's time to start wisely using the accumulated basic information, which we will supplement as necessary.
Let us recall that in this chapter we are looking for the humoral components of hypertension that increase vascular tone and blood pressure. These are blood chemicals. Of these, angiotensin II is considered in medicine to be a particularly hypertensively dangerous substance, which, along with a very strong chemical increase in vascular tone, also preserves the volume of blood circulating in the vessels. This last consideration is of utmost importance, and the literature always emphasizes the hypertensive danger of angiotensin II.
The first step in our search will be to exclude from consideration all vasodilatory blood chemicals. It is believed that they do not take part in increasing vascular tone and blood pressure. Neither acetylcholine, nor histamine, nor bradykinin, nor prostaglandins were noted to increase blood pressure. All researchers are unanimous in this. The vasoconstrictor chemicals in the blood remain in our field of vision: adrenaline, norepinephrine, vasopressin, angiotensin II, serotonin.
But serotonin, despite its name, does not have the desired properties and we exclude it from consideration. The opinion on this matter is unanimous. We will devote the next chapter to adrenaline and norepinephrine.
