Nervous Regulation of Heart rate in animals
Sympathetic and parasympathetic divisions of ANS play a key role in the regulation of heart rate. The nerves regulate to a larger extent the rate rather than the force of contraction either directly or indirectly.
The two atria are especially well supplied with large number of both sympathetic and parasympathetic nerves, but the ventricles are supplied mainly by sympathetic nerves and fewer parasympathetic fibres.
Direct nervous control
Cardiac activity is regulated by cardio accelerator (augmentor) nerves and cardio inhibitory nerves.
Cardio accelerator nerve fibres
Sympathetic nerves to the heart originate as post ganglionic fibres from the inferior, middle and superior cervical and first 4-5 thoracic ganglia, run along with vagus to form the cardiac nerves and plexus which pass to the heart along with great veins and arteries.
Sympathetic division of the ANS provides two sets of accelerator fibres, the vago-sympathetic fibres, originating from the cervical ganglion and run along the vagal fibres and the cardio sympathetic fibres from the 2, 3, 4, 5th thoracic nerves which function in emergency. Neurotransmitter of the sympathetic system is nor-epinephrine, which mainly act through b1-receptors.
Sympathetic fibres supply the atria, S.A. node, A.V. node and the ventricles stimulation of which causes increase heart rate and force of contraction referred to as positive chronotropic and positive inotrophic effects, respectively.
Cardio inhibitory nerve fibres
Vagus, the Xth cranial nerve is the parasympathetic nerve originates from the dorsal nucleus of the medulla, form cardiac plexus with sympathetic nerves of the cervical ganglia. Vagus descends along with sympathetic fibres and terminates on the S.A. node in mammals and ventricles in amphibians.
In mammals, vagus supplies fibres to the S.A. node, atrial muscles, A.V. node and A.V. bundle. The vagus nerve on stimulation produces inhibitory effect on heart resulting in negative chronotropic and negative inotropic effects. The inhibitory effect is more by right vagus than the left because SA node receives more fibres from the right vagus.
Stimulation of vagus results in complete inhibition of heart beat (vagal inhibition) for a short duration. Following this the ventricles, start weak contractions called the vagal escape due to the shifting of the pacemaker from S.A. node to ventricular site, the ectopic foci.
Principally, parasympathetic stimulation causes a marked decrease in heart rate and a slight decrease in contractility. Both the sympathetic and parasympathetic fibres of ANS constantly discharge impulses to the heart to keep the heart in tonic state.
Under normal resting state, the parasympathetic nerves to heart are in tone. Vagal tone is particularly more in athletic animals. Hence, the heart rate is slower in athletic animals.
Cutting the vagi accelerates heart rate. The sympathetic nerves are more functional only during emergency to meet excessive O2 and nutrients demand of the metabolically active tissues. Stimulation of sympathetic fibres increases the heart rate, tachycardia and parasympathetic decreases heart rate, bradycardia.
Indirect nervous control of heart
Indirect nervous control of cardiac activity is principally mediated by reflex mechanisms, which are essential for the maintenance of blood pressure (BP). The reflexes are of two groups- Cardio accelerator reflex (Bain bridge reflex) and Cardio inhibitory reflex.
Cardio accelerator reflex (Bain bridge reflex)
When the blood volume in the right side of the heart has increased with accumulation of blood, the stretch receptors of the right atrial wall get excited and the impulses are carried through vagus to the vasomotor centre of the medulla.
It causes inhibition of the vagal tone to the heart, but stimulates the vasoconstrictor centre. This result in increased force of contraction of the heart and constriction of the blood vessels, the BP returns to normal.
Cardio inhibitory reflex
The two baroreceptors, the carotid sinus and the aortic body are very sensitive to increased BP and play a key role in the regulation of BP and heart rate.
Carotid sinus, pressure sensitive stretch receptors is located at the bifurcation of the internal and external carotid artery sense the BP changes and transmits the sensory impulses to cardio inhibitory area of the vasomotor centre of the medulla through afferent nerve, the sinus nerve, a branch of the glossopharyngeal nerve.
Aortic body pressure receptors is the thickened portion of the aortic arch get stimulated by increase in BP and the impulses are transmitted through aortic or cardio depressor nerve, a branch of vagus to the cardio inhibitory area of the medulla.
On stimulation of these two receptors by increased BP, inhibits vascular sympathetic nerves resulting in vasodilatation. The efferent impulses from cardio inhibitor centres pass through vagus causes reduction in heart rate and also vasodilatation. The sinus and aortic nerves are called as buffer nerves.
The signals regarding the drop in BP are transmitted to cardio accelerator area of the vasomotor centres of the medulla causes inhibition of the activities of cardio inhibitor centres, whereas the cardio accelerator centre and the sympathetic division are stimulated resulting in vasoconstriction and increased heart rate.