Cardiovascular Regulatory Mechanisms


In humans and other mammals, multiple cardiovascular regulatory mechanisms have evolved. These mechanisms increase the blood supply to active tissues and increase or decrease heat loss from the body by redistributing the blood. In the face of challenges such as hemorrhage, they maintain the blood flow to the heart and brain. When the challenge faced is severe, flow to these vital organs is maintained at the expense of the circulation to the rest of the body

Innervation of the blood vessels

Sympathetic noradrenergic fibers end on blood vessels in all parts of the body to mediate vasoconstriction. In addition to their vasoconstrictor innervation, resistance vessels in skeletal muscles are innervated by vasodilator fibers, which, although they travel with the sympathetic nerves, are cholinergic (sympathetic cholinergic vasodilator system). There is no tonic activity in the vasodilator fibers, but the vasoconstrictor fibers to most vascular beds have some tonic activity. When the sympathetic nerves are cut, the blood vessels dilate. In most tissues, vasodilation is produced by decreasing the rate of tonic discharge in the vasoconstrictor nerves, although in skeletal muscles it can also be produced by activating the sympathetic cholinergic vasodilator system

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Cardiac innervation

Impulses in the sympathetic nerves to the heart increase the cardiac rate, rate of transmission in the cardiac conductive tissue, and the force of contraction (inotropic effect). They also inhibit the effects of vagal parasympathetic stimulation, probably by the release of neuropeptide Y, which is a transmitter in the sympathetic endings. Impulses in vagal fibers decrease heart rate.

A moderate amount of tonic discharge takes place in the cardiac sympathetic nerves at rest, but there is a good deal of tonic vagal discharge (vagal tone) in humans and other large animals. After the administration of parasympatholytic drugs such as atropine, the heart rate in humans increases from 70, its normal resting value, to 150 to 180 beats/min because the sympathetic tone is unopposed. In humans in whom both noradrenergic and cholinergic systems are blocked, the heart rate is approximately 100 beats/min

Cardiovascular control

The cardiovascular system is under neural influences coming from several parts of the brain, which in turn receive feedback from sensory receptors in the vasculature. A simplified model of the feedback control circuit. An increase in neural output from the brain stem to sympathetic nerves leads to a decrease in blood vessel diameter (arteriolar constriction) and increases in stroke volume and heart rate, which contribute to a rise in blood pressure. This in turn causes an increase in baroreceptor activity, which signals the brain stem to reduce the neural output to sympathetic nerves.


The baroreceptors are stretch receptors in the walls of the heart and blood vessels. The carotid sinus and aortic arch receptors monitor arterial circulation. Receptors are also located in the walls of the right and left atria at the entrance of the superior and inferior venae cavae and the pulmonary veins, as well as in the pulmonary circulation. These receptors in the low-pressure part of the circulation are referred to collectively as the cardiopulmonary receptors

Baroreceptor nerve activity

Baroreceptors are more sensitive to pulsatile pressure than to constant pressure. A decline in pulse pressure without any change in mean pressure decreases the rate of baroreceptor discharge and provokes a rise in systemic blood pressure and tachycardia. At normal blood pressure levels (about 100 mm Hg mean pressure), a burst of action potentials appears in a single baroreceptor fiber during systole, but there are few action potentials in early diastole. At lower mean pressures, this phasic change in firing is even more dramatic with activity only occurring during systole. At these lower pressures, the overall firing rate is considerably reduced.

Direct effects on the role

When intracranial pressure is increased, the blood supply to RVLM neurons is compromised, and the local hypoxia and hypercapnia increase their discharge. The resultant rise in systemic arterial pressure tends to restore the blood flow to the medulla and over a considerable range, the blood pressure rise is proportional to the increase in intracranial pressure. The rise in blood pressure causes a reflex decrease in heart rate via arterial baroreceptors. This is why bradycardia rather than tachycardia is characteristically seen in patients with increased intracranial pressure.


Baroreceptor nerves terminate in the NTS and release glutamate. NTS neurons project to the CVLM and nucleus ambiguous and release glutamate. CVLM neurons project to RVLM and release GABA. This leads to a reduction in sympathetic activity and an increase in vagal activity.

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