Download Nerve and humoral regulation of heart activity

Nerve and humoral
regulation of heart activity.
Physiology of systemic
circulation regulation
Effects of nn. vagi
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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 alfaadrenoreceptors, which are most
spread in major coronary vessels.
Transmission impulses through betaadrenergic 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.
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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.
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Location of receptors in the heart
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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
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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.
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Baroreceptor reflexes
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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.
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Mechanisms of heart auto
regulation
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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. Lowpressure 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.
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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.
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Central link
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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.
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Reflexes from proprio-, termoand 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.
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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.
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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.
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Humoral regulation of heart
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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
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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
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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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