Control of heart rateEdexcel A-Level Biology B: Revision notes

The sinoatrial node (SAN) in the wall of the right atrium is myogenic: it generates waves of excitation without any nervous input, setting an intrinsic rate of about 100 beats per minute. The autonomic nervous system adjusts this rate to match the body's needs. It works without conscious control and has two branches that act on the SAN in opposite ways.

Baroreceptors in the aortic arch and carotid sinus detect stretching of the artery wall, so they monitor blood pressure. Chemoreceptors in the carotid bodies and aorta detect a fall in blood pH (a rise in carbon dioxide and H⁺ concentration) and, to a lesser extent, a fall in oxygen. Both types send impulses to the cardiac centre in the medulla oblongata.

The cardiac centre contains two areas: one increases heart rate and one decreases it. It integrates the incoming impulses and sends impulses to the SAN along the autonomic nerves.

The sympathetic nerve carries impulses from the cardiac centre to the SAN. Its endings release noradrenaline, which makes the SAN fire more often and increases heart rate.

The parasympathetic nerve (the vagus nerve) also supplies the SAN. Its endings release acetylcholine, which makes the SAN fire less often and decreases heart rate. At rest the parasympathetic effect dominates, holding the rate to about 70 beats per minute rather than the SAN's intrinsic rate of about 100.

Exercise: muscles respire faster, blood CO₂ rises and pH falls. Chemoreceptors send more impulses to the cardiac centre, which increases sympathetic impulses to the SAN. Heart rate and cardiac output rise, so CO₂ is removed faster.

Fall in blood pressure: baroreceptors send fewer impulses, so sympathetic stimulation rises and the heart rate increases.

Rise in blood pressure: baroreceptors send more impulses, so parasympathetic stimulation rises and the heart rate falls.

Each is negative feedback: the change is detected, the effector (SAN) responds and the original condition is restored.

In stress or danger, sympathetic stimulation causes the adrenal glands to release adrenaline into the blood. Adrenaline travels to the SAN and increases heart rate. Because it is carried in the blood, the effect begins more slowly than a nerve impulse and lasts longer, until the adrenaline is broken down.

A denervated heart (for example after a transplant) shows both routes at work: with the nerves cut, the resting rate is the SAN's intrinsic rate of about 100 beats per minute, and the rate rises only slowly during exercise through adrenaline alone.