Describe briefly how the sino-atrial node acts as the pacemaker of the heart. Give a short account of the regulation of heart rate.

Outline:

·        Conducting system of heart

·        Pacemaker potential generation

·        Autonomic control of heart rate

Essay:

            The heart is endowed with a specialized conducting system that generates rhythmical impulses to cause rhythmical contraction of the heart muscle and conducting these impulses rapidly throughout the heart. The components of this conducting system are the sinoatrial node (SA node), the internodal atrial pathways, the atrioventricular node (AV node), the atrioventricular bundle and its branches, and the Purkinje system. The SA node is the normal cardiac pacemaker – its rate of discharge determines the rate at which the heart beats. Impulses generated in the SA node pass through the atrial pathways to the AV node, through this node to the AV bundle and via the Purkinje system to the ventricular muscle.

            The SA node is located in the superior lateral wall of the right atrium immediately below and lateral to the opening of the superior vena cava. The SA node has a membrane potential, that after each impulse, rises to the firing level (become less negative). This resting membrane potential is due to the high extracellular sodium concentration which enhances its leakage into the sinus nodal fibers and to the number of already open sodium channels present in the resting nodal fibers. The cell membranes of the sinus nodal fibers contain fast sodium channels and slow calcium-sodium channels. When the continual increase in resting membrane potential reaches a threshold voltage of –40mV, the slow calcium-sodium channels and the fast sodium channels are activated, leading to rapid entry of both sodium and calcium ions. This generates an action potential which spreads via the interatrial pathways to the AV node which transmits it to the rest of the conducting system, causing the myocardium to contract. Repolarization is caused by inactivation of the fast sodium channels and slow calcium-sodium channels and the opening of potassium channels which allow for efflux of large quantities of potassium ions. After closing of the potassium channels, the inward-leaking sodium ions once again overbalance the outward of potassium ions, causing the membrane potential to increase once more.

            The heart rate must be tightly regulated to ensure that blood flow to the tissues commensurate with its metabolic activities. The nodal fibers are innervated by both parasympathetic and sympathetic nerve fibers and are therefore under autonomic control. Acetylcholine released at the parasympathetic nerve endings increases potassium conductance of nodal tissue. This action is mediated by muscarinic receptors, which via a G protein, open a special set of potassium channels. The resulting efflux of potassium counters the rising membrane potential due to the influx of sodium ions. The result is a decrease in the rate of rhythmic discharge of the SA node and a decrease in the excitability of the AV bundle fibers, thereby slowing transmission of the cardiac impulse into the ventricles, decreasing the heart rate. Normally the tonic control of heart rate is dominated by the parasympathetic nervous system.

            On the other hand, stimulation of the sympathetic cardiac nerves makes the membrane potential increases more rapidly, and the rate of spontaneous discharge increases. Norepinephrine secreted by the sympathetic endings bind to b₁ receptors, and the resulting increase in cAMP facilitates the opening of the sodium and calcium channels. This accelerates the rhythmic discharge of the SA node and the rate of conduction of the impulses, increasing the heart rate.

            The center of control of autonomic discharge is exerted by groups of neurons in the medulla that are collectively called the vasomotor center. The afferent input to the vasomotor center comes from the baroreceptors, chemoreceptors, the cortex and hypothalamus. The baroreceptors are stretch receptors in the walls of the heart and blood vessels. Impulses generated in the baroreceptors inhibit the tonic discharge of the sympathetic nerves and excite the vagal innervation of the heart, resulting in a decrease in heart rate. Activation of chemoreceptors, due to hypoxia or hypercapnia, however, increases the rate of discharge of the sympathetic nerves, increasing the heart rate. There are descending tracts to the vasomotor center from the cerebral cortex that relay in the hypothalamus. These fibers are responsible for the increase in heart rate produced by emotions such as sexual excitement and anger. Other emotions such as fear and grief lowers the heart rate.