Nerve and humoral regulation of heart activity Nerve and humoral regulation of heart activity. Physiology of systemic circulation regulation

Effects of nn. vagi Effects of nn. vagus on the heart activity. Parasympathetic stimulation causes decrease in heart rate and contractility, causing blood flow to decrease. It is known as negative inotropic, dromotropic, bathmotropic and chronotropic effect.

Sympathetic effects Sympathetic nerves from Th1-5 control activity of the heart and large vessels. First neuron lays in lateral horns of spinal cord. Second neuron locates in sympathetic ganglions. Sympathetic nerve system gives to the heart vasoconstrictor and vasodilator fibers. Vasoconstrictor impulses are transmitted through alfa-adrenoreceptors, which are most spread in major coronary vessels. Transmission impulses through beta-adrenergic receptors lead to dilation of small coronary vessels. Sympathetic influence produces positive inotropic, chronotropic, dromotropic, bathmotropic effects, which is increase of strength, rate of heartbeat and stimulating excitability and conductibility also.

Control of heart activity by vasomotor center Lateral portion of vasomotor center transmit excitatory signals through sympathetic fibers to heart to increase its rate and contractility. Medial portion of vasomotor center transmit inhibitory signals through parasympathetic vagal fibers to heart to decrease its rate and contractility. Neurons, which give impulses to the heart, have constant level of activity even at rest, which is characterized as nervous tone.

Location of receptors in the heart Heart muscle contains, both chemical and stretch receptors in coronary vessels, all heart cameras and pericardium. Stretch receptors are irritated by changing blood pressure in heart cameras and vessels. Chemo sensitive cells, which are stimulated by decrease O2, increase of CO2, H+ and biological active substances also, are called as chemoreceptors.

Reflexes from atria When atria pressure increase due to increasing blood volume, atria stretched. Signals pass to afferent arterioles in kidneys to cause vasodilatation and glomerullar capillary pressure, thereby increasing glomerullar filtration. Signals also pass to hypothalamus to decrease antidiuretic hormone secretion and so fluid reabsorbtion. It causes decreasing both blood volume and arterial pressure to normal. Other reflex reaction is known as atria and pulmonary artery reflex. When atria pressure increase due to increasing blood volume, atria stretched. Low-pressure receptors, similar to baroreceptors, in atria and pulmonary arteries stretched and stimulated. Signals pass to vasomotor center and inhibit vasculomotor area. Arterial pressure decreases to normal.

Reflex reactions from receptors of pericardium, endocardium and coronary vessels Reflex reactions from receptors of pericardium, endocardium and coronary vessels lead to stimulation n. vagus. It leads to parasympathetic stimulation of the heart. Parasympathetic stimulation causes decrease in heart rate and contractility, causing blood flow to decrease. It is known as negative inotropic, dromotropic, bathmotropic and chronotropic effect.

Baroreceptor reflexes Increasing arterial pressure stretched and stimulated baroreceptors in carotid sinus and aortic arc. Signals pass through glossopharyngeal and vagal nerve to tractus solitarius in medulla. Secondary signals from tractus solitarius inhibit vasoconstrictor center and excite vagal center. Peripheral vasodilatation and decrease both heart rate and contractility occur. Arterial pressure decreases to normal. When arterial pressure decreases, whole process occurs, causing opposite result.

Irritation of visceroreceptors Irritation of visceroreceptors results in stimulation of vagal nuclei, which cause decreasing blood pressure and heartbeat. Parasympathetic stimulation causes decrease in heart rate and contractility, causing blood flow to decrease. It is known as negative inotropic, dromotropic, bathmotropic and chronotropic effect. This mechanism is important for doctor in performing diagnostic procedures, when probes from apparatuses are attached into visceral organs. This may cause excessive irritation of visceral receptors.

Mechanisms of heart auto regulation Greater rate of metabolism or less blood flow causes decreasing O2 supply and other nutrients. Therefore rate of formation vasodilator substances (CO2, lactic acid, adenosine, histamine, K+ and H+) rises. When decreasing both blood flow and oxygen supply smooth muscle in precapillary sphincter dilate, and blood flow increases. Moderate increasing temperature increases contractile strength of heart. Prolonged increase of temperature exhausts metabolic system of heart and causes cardiac weakness. Anoxia increases heart rate. Moderate increase CO2 stimulates heart rate. Greater increase CO2 decreases heart rate.

Atria and pulmonary artery reflex When arterial pressure increases due to increasing blood volume, atria stretched. Low-pressure receptors, similar to baroreceptors, in atria and pulmonary arteries stretched and stimulated. Signals pass to vasomotor center and inhibit vasculomotor area. Arterial pressure decreases to normal. Excessive stretching of lung tissue causes excitation of n. vagus. It leads to parasympathetic stimulation of the heart. Parasympathetic stimulation causes decrease in heart rate and contractility, causing blood flow to decrease.

Afferent link Nerve receptors, which are capable react to changing blood pressure, lays in heart cameras, aorta arc, bifurcation of large vessels as carotid sinus and other parts of vascular system. Irritation of these mechanical receptors produce nerve impulses, which pass to higher nerve centers for processing sensory information from visceral organs.

Central link Vasoconstrictor area of vasculomotor center is located bilaterally in dorsolateral portion of reticular substance in upper medulla oblongata and lower pons. Its neurons secrete norepinephrine, excite vasoconstrictor nerves and increase blood pressure. It transmits also excitatory signals through sympathetic fibers to heart to increase its rate and contractility. Vasodilator area is located bilaterally in ventromedial of reticular substance in upper medulla oblongata and lower pons. Its neurons inhibit dorsolateral portion and decrease blood pressure. It transmits also inhibitory signals through parasympathetic vagal fibers to heart to decrease its rate and contractility. Posterolateral portions of hypothalamus cause excitation of vasomotor center. Anterior part of hypothalamus can cause mild inhibition of one. Motor cortex excites vasomotor center. Anterior temporal lobe, orbital areas of frontal cortex, cingulated gyrus, amygdale, septum and hippocampus can also control vasomotor center.

Efferent link Stimulation of sympathetic vasoconstrictor fibers through alfa-adrenoreceptor causes constriction of blood vessels. Stimulation of sympathetic vasodilator fibers through beta-adrenoreceptors as in skeletal muscles causes dilation of vessels. Parasympathetic nervous system has minor role and gives peripheral innervations for vessels of tong, salivatory glands and sexual organs.

Reflexes from proprio-, termo- and interoreceptors Contraction of skeletal muscle during exercise compress blood vessels, translocate blood from peripheral vessels into heart, increase cardiac output and increase arterial pressure. Stimulation of termoreceptors cause spreading impulses from somatic sensory neurons to autonomic nerve centers and so leads to changing tissue blood supply. Irritation of visceroreceptors results in stimulation of vagal nuclei, which cause decreasing blood pressure and heartbeat.

Regulation of blood flow in physical exercises In physical exercises impulses from pyramidal neurons of motor zone in cerebral cortex passes both to skeletal muscles and vasomotor center. Than through sympathetic influences heart activity and vasoconstriction are promoted. Adrenal glands also produce adrenalin and release it to the blood flow. Proprioreceptor activation spread impulses through interneurons to sympathetic nerve centers. So, contraction of skeletal muscle during exercise compress blood vessels, translocate blood from peripheral vessels into heart, increase cardiac output and increase arterial pressure. Regulation of blood flow in physical exercises

Cardiovascular Adjustments to Exercise

Anrep's effect Increase of blood flow in aorta and so coronary arteries leads to excessive stretching surrounding myocardial cells. According to Frank Starling low cardiac contraction is directly proportional to initial length of its fibers. So increase of coronary blood flow leads to stimulation heartbeat.

Boudichi phenomenon In evaluation heart beat rate increase of every next heart contraction is observed. It caused by rising of Ca2+ influx into myocardial cells without perfect outflow, because of shortening of cardio cycle duration.

Humoral regulation of heart Effects of thyroid hormones Thyroid hormones increase transmission process in ribosome and nucleus of cells. Intracellular enzymes are stimulated due to increasing protein synthesis. Also increases glucose absorption and uptake of glucose by cells, increases glycolisis and gluconeogenesis. In blood plasma increases contents of free fatty acids. All these effects of thyroid hormones lead to increase activity of mitochondria in heart cells and ATP formation in it. So, both activity of heart muscle and conduction of impulses are stimulated.

Endocrine function of heart Myocardium, especially in heart auricles capable to secretion of regulatory substances as atria Na-ureic peptide, which increases loss of Na+ in increase of systemic pressure, or digitalis-like substances, which can stimulate heart activity.

Effects of acetylcholin Effects of acetylcholin leads to increase of K+ permeability through cell membrane in conductive system, which leads to hyper-polarisation and cause such effects to the heart activity: - Negative inotropic effect - decreasing strength of heart contractions; - Negative chrono-tropic effect - decreasing heartbeat rate; -Negative dromo-tropic effect - decreasing heart conductibility; - Negative bathmo-tropic effect - decreasing excitability of heart muscle.

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