Nerve and humeral regulation of heart activity
Key words and phrases: endocrine regulation, catecholamynes, alpha- and bita-adrenoreceptors, adrenalin, noradrenalin, inotropic effect, chrono-tropic effect, dromo-tropic effect, bathmo-tropic, excitability of heart muscle, effects of thyroid hormones, effects of adrenocortical hormones, insulin, glucagone, incretory function of heart, atria Na-ureic peptide, decreasing O2 supply, increase CO2, metabolic effects, Frank Starling effect.
Central nervous regulation of heart activity, regulation of blood flow, pumping activity of the heart, control of arterial pressure, cerebral cortex control heart activity, behavioral reactions, somatic sensory zone, premotor cortex, heart activity, hypothalamus, parasympathetic control of heart activity, sympathetic nervous system, efferent innervations of the heart, vagal innervations of the heart, inotropic, dromotropic, bathmotropic, chronotropic effect, reflexes from extracardial receptors and baroreceptor reflexes.
Mechanisms of heart regulation
The aim of the circulatory regulation is to regulate the blood flow of organs to fit their metabolic requirement in different condition.
The regulation of blood flow are of three major types:
1. Neural
2. Humoral
3. Local
1. CARDIAC INNERVATION:
Sympathetic nerve – noradrenergic fiber;
Parasympathetic nerve – cholinergic fiber
Noradrenergic sympathetic nerve
● to the heart increase the cardiac rate (chronotropy effect)
● the force of cardiac contraction (inotropy effect).
Cholinergic vagal cardiac fibers decrease the heart rate.
2. HUMORAL REGULATION
a) Effects of catecholamynes are transmitted by alfa– and bita-adrenoreceptors.
Adrenalin and noradrenalin stimulate heat activity and cause positive regulatory effects:
– Positive inotropic effect – increasing strength of heart contractions;
– Positive chrono-tropic effect – increasing heartbeat rate;
– Positive dromo-tropic effect – increasing heart conductibility;
– Positive bathmo-tropic effect – increasing excitability of heart muscle.
Nor-epinephrine increases permeability of cardiac fiber membrane to Na+ and Ca2+.
b) 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.
c) Effects of ions:
-Ca2+ causes spastic contraction of heart. Decreasing Ca2+ causes cardiac flaccidity.
Excessive concentration of K+ causes decreasing heart rate. Impulse’ transmission through AV bundle is blocked. If K+ level was previously decreased, increasing Concentration of K+ capable normalize cardiac rhythm. Na+ competes Ca2+ in contractile process. So increasing Na+ may depress cardiac contraction.
d) 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.
e) Effects of adrenocortical hormones. Aldosterone causes increasing Na+ and Cl– in blood and decreases K+. This is actually for producing action potential in the heart. Cortisol stimulates gluconeogenesis and increase blood glucose level. Amino acids blood level and free fatty acids concentration in blood increases also. Utilization of free fatty acids for energy increases. These mechanisms actual in stress reaction. So heart activity is stimulated.
f) Hormones of islets of Langerhans effects. Insulin promotes facilitated diffusion of glucose into cells by activation glucokinase that phosphorilates glucose and traps it in the cell, promotes glucose utilization, causes active transport of amino acids into cells, promote translation of mRNA in ribosome to form new proteins. Also insulin promotes glucose utilization in cardiac muscle, because of utilization fatty acids for energy. Clucagone stimulate gluconeogenesis, mobilizes fatty acids from adipose tissue, promotes utilization free fatty acids foe energy and promotes gluconeogenesis from glycerol. So both hormones can increase strength of heartbeat.
g) 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.
2. Mechanisms of heart auto regulation
a) 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.
b) Intrinsic regulation is performed in response changes of blood volume, flowing into the heart. It is known as Frank Starling low. Within physiological limits heart pumps all blood that comes to it without allowing excessive damming of blood in veins. Cardiac contraction is directly proportional to initial length of its fibers. In end-diastolic volume over 180 ml excessive stretching heart fibers occurs and strength of next cardiac contraction decreases.
c) Anrep’s low. 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.
d) 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.
3. General characteristic of central nervous regulation of heart activity.
Central nervous system affects regulation of blood flow and pumping activity of the heart and provides very rapid control of arterial pressure. Cerebral cortex control heart activity to correct it depending on body needs when performing behavioral reactions. Secondary somatic sensory zone takes part in analysis of afferent information from the hart. Pre-motor cortex may correct heart activity by descendant influences through hypothalamus. Anterior hypothalamus promotes parasympathetic control of heart activity. Posterior hypothalamus realizes their effects through sympathetic nervous system.
4. Efferent innervations of the heart.
a) Specialties of vagal innervations of the heart. Right n. vagus controls mainly right atrium and SA node. Left n. vagus control AV node, His bundle and all contractile myocardium. So irritation of right nerve causes bradycardia. Effects of left nerve lead to decrease of contractility and conductibility.
b) 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.
c) 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.
d) 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.
5. Reflex regulation of heart activity from heart receptors.
a) 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.
b) 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.
c) Reflex reactions from receptors of pericardium, endocardium and coronary vessels lead to stimulatio. 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.
6. Reflexes from extracardial receptors.
a) Baroreceptor reflexes. In the reflex regulation of the heart are important reflexes arising from receptors of the primary part. Mechanoreceptors excited when of aortic artery walls expands (during fillig heart with blood). As a result –bradycardia arise. Descending of aortic wall leads to an increase of heart rate. Mechanoreceptors are present also in the large arteries. The effect is the same as with the receptors of the aorta, but much less expressed. Normally, these effects overlapped by reflections from the aortic arch.
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
b) 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.
c) Regulation of heart activity during physical exercises. Motor areas of cerebral cortex are activated to cause exercise most of reticular activating system is also activated. Increase stimulation of vasoconstrictor and cardio acceleratory areas of vasomotor center leads to increasing arterial pressure. Contraction of skeletal muscles during exercises cause compression of blood vessels. It leads to translocation blood from peripheral vessels into heart. Cardiac output increases, because of rising arterial pressure.
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.
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.
Nota bene: Irritation of thrigeminal nerve, otherwise leads to excitation vagal nucleus through interneuronal connection. So, parasympathetic effects develop.
d) 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.
3. MECHANISMS OF HEART AUTOREGULATION
Changes of intracellular metabolic processes in the heart:
Intracellular metabolism in cardiomyocytes characterized by cycles of metabolic processes associated with cardiac activity. The fastest decay of energy-rich compounds – ATP and glycogen – is at the time of systole and on electrocardiogram registeres as QRS-complex . Resynthesis and recovery of these substances is in diastole In addition, for rebuilding of structures, damaged during systole and restoring ionic balance, there is increased protein synthesis (in diastole).
Depending on the activity, cardiomyocytes can selectively adsorb from blood and accumulate in their cytoplasm substances, that maintain and regulate their bioenergy.
Functio of increcion:
In the right atrium, atrial natriuretic peptide which has a direct depressant effect on myocardial contractility is produced. It also inhibits the activity of the sympathetic nervous system and inhibits the release of catecholamines. When it comes into the the hollow veins (vena cava), pulmonary trunk and aortic arch, sensitivity of receptors of vagal afferent fibers, located there, increases. Id leads to increase of parasympathetic influences on the heart.
Also in the myocardium so-called braiatriuretic peptide produses (was first detected in the NUP). With an increase of blood volume and hipernatriyaemia this hormone inhibits transmembrane sending of the sodium ions, inhibits the activity of Na + / K +- pump, namely stimulates the effects of cardiac glycosides.
Therefore, braiatriuretic peptide was also called “dihitalioid factor”. It increases myocardial contractility .
● 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.
Nota bene: 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.
