Download 28 Neural mechanism of heart` regulation

Neural mechanism of
heart’ regulation
Nerve and humeral regulation of heart
activity. Physiology of systemic
circulation regulation
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:
Neural
Humoral
Local
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.
The mechanism of catecholamines action on the heart
Catecholamines, interacting with
β-adrenoceptors of heart,
cause activation of enzyme
adenylatecyclase, which
converts adenosinetryfosforic
acid in cyclic
adenosinemonophosphate
(cAMP).
Increasing of intracellular concentration of cAMPh
causes activation of cAMPhdependent proteinkinase, which
catalyzes the phosphorylation
of proteins. It leads to an
increase in entrance of sodium
and calcium into the cell.
noradrenalin
adrenoreceptor
adenylate
cyclase
cytoplasm
ATPh
Not active
proteinkinase
cAMPH
Activeted proteinkinase
sarcoplasmic
reticulum
Increasisng of strength
of heart contractions
troponin
Catecholamines
The action of acetylcholine on the activity of the heart
(Effects of n. vagus on the heart)
In the external membrane of cardiomyocytes
muscarinic (M)-cholinergic receptors are
dominated. Similarly as β-adrenoceptors, density
of muscarinic receptors in the myocardium
depends on the concentration of their
antagonists.
During interaction with muscarinic receptors
Acetylcholine primarily couses inhibition of
Adenylate-cyclase activity and secondary –
activates Guanylate-cyclase (GC).
The GC converts Huanozyn-tryfosfat into the
Cyclic Guanosine-monophosphate (cGMP).
Increase of intracellular concentration
of cGMP causes activation of Acetylcholine
dependent potassium channels. It leads to
increase the of potassium ions out of
the cardiomyocytes. Due to increased release of
potassium occurs hyperpolarization of cell
membranes.
Efects:
1. negative inotropy
2. negative chronotropy
3. negative dromotropy
4. negative batmotropy
acethylholine
M-cholinergic
receptors
Hyperpolarizatin
of membrane
inhibition
GC
cytoplasm
ATP
cGMP
cAMP
proteincinase
Frank-Starling law

Frank experiments on frog
heart has found that
ventricular output
increases with the increase
of saline pressure, which
stretches the ventricular
cavity. Starling showed on
isolated dog hearts that the
more ventricles are
stretched by blood during
diastole, the more their
reduction in the next
systole.
Resistance
regulation
Compresion
camera
ce
Lung
Venois
reservoir
Compression
in aorta
filling
pressure
Ventriculus volume
Scheme of heart-lung
aparate by Starling
The essence of the Frank-Starling law
As a result the "law of the heart" (FrankStarling law or heterometryc mechanism
of regulation) was derived: the force of
myocardial contraction fibers depends on
their end-diastolic length.
From the heart of the law implies that
increased filling of the heart with blood
leads to increased force of heart
contractions. Reducing of the force of
myocardial contraction observed when it
stretched more than 25% of the initial
length. Such stretching is absent in the
healthy heart (only 20%).
So, this act, means that the number of
bridges of aktynomioze is the maximal
during strain of each sarcomere to 2.2
microns. And force of cardiac contraction
will depend on the number of formed
bridges.
the Frank-Starling law
Actine – Act
Myosine – My
stretching of the sarcomere
Act
S
T
R
E
I
N
My
FO
R
CE
time
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.
Bainbridge Reflex
Increased Intravascular Volume
Atrial Stretch Receptors
Medullary Activation (via Vagus
Nerve)
Increased Sympathetic
Activity to SA Node
Direct Stretching
of SA Node
Increased
Heart Rate
Effect of the cerebral cortex on heart
activity
Cortex is the organ of
mental activity. It provides a
holistic adaptive response. The
work of the heart depends on
the functional state of the
cerebral cortex. Thus, in
athletes observed pre-start
condition manifesting with
increasing of heart rate.
Overpassing anxiety state
reduction of it can be achieved.
The effects of stimulation of the
cerebral cortex occur during
stimulation of motor and
premotor zones, cingulate
gyrus , orbital surface of the
frontal lobe, the anterior region
of the temporal lobe. Usually an
increase of heart rate observed
herewith.
Cortex
Hypothalamus
AVnode
Medulla
SAnode
Cord
Symphatic
cardiac nerves
paravertebral symphatic ganglia
Effects of the hypothalamus on heart activity
During stimulation of
different areas of the
hypothalamus in
anesthetized animals
special points were
detected. Stimulation of
them accompanied by
changes of the frequency
and force of heart
contractions. Thus, in
hypothalamus are
structures that regulate
the activity of the heart.
Often, but not always,
electrical stimulation of the
anterior hypothalamus
leads to decreased
cardiac and rear – to
increase heart rate.
Cortex
Hypothalamus
AVnode
Medulla
SAnode
Cord
Symphatic
cardiac nerves
paravertebral symphatic ganglia
Cardiovascular centers of the brainstem
Medulla
oblongata is
essential to
Cardiovascuar
centers.
Peculiaritiesof the vagal innervation of the heart
In the medulla oblongata the nucleus of
vagus nerve located. The axons of the
cells of the nucleus within the right and
left nerve trunks sent directed to the heart
and form synapses on motor metasympatyc
neurons.
Medulla
Right vagus nerve fibers are distributed
mainly in the right atrium. The associated
neurons inervate myocardium, coronary vessels
and sinus-atrial node. As a result of the
structural features of the right vagus nerve
stimulation of it shows its influence on heart
rate.
AVnode
N. vagus
SAnode
Efects:
1. negative inotropy
2. negative chronotropy
3. negative dromotropy
4. negative batmotropy
Left vagus nerve fibers transmit their effects to atrioventricular node. As a result
of the structural features of the left vagus nerve stimulation of it shows its
influence on atrioventricular conduction and contractility of cardiomyocytes
(heart rate effect).
Effects of n. vagus

Effects of n. 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.
Influence of sympathetic nervous system
activity of the heart
The first neurons of the
sympathetic nerves that transmit
impulses to the heart, located in
the lateral horns of the upper four
or five thoracic segments of the
spinal cord (Th1-Th5).
Processes of these neurons
terminate in the cervical and upper
thoracic sympathetic nodes, where
the latter neurons, processes
which go to the heart.
Cortex
Medulla
Cord
Efects:
1. positive inotropic
2. positive chronotropic
3. positive dromotropic
4. positive batmotropnyy
AVnode
Hypothalamus
SAnode
Symphatic
cardiac nerves
paravertebral symphatic ganglia
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.
Adrenergic receptors
Epinephrine
Norepinephrine
α1 receptor on vessels
Vasoconstriction
β1 receptor on heart
Positive effect
β2 receptor on vessels
(skeletal muscle and liver)
Vasodilation
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 and innervation of arterial baroreceptors
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