MECHANISMS INVOLVED OVERALL CONTROL OF BLOOD PRESSURE

Baroreflex Control of Blood Pressure

The arterial baroreceptor reflex is the primary mechanism for the short-term or rapid control of arterial blood pressure, whereas neurohumoral factors (predominantly the control of sodium excretion) are responsible for long-term or slower control.

ARTERIAL BARORECEPTOR RESPONSE TO DECREASED ARTERIAL PRESSURE

A decrease in blood pressure may be the result of loss of blood (hemorrhage) or a shift in blood away from the heart (standing up). In response to a decrease in arterial pressure, the baroreceptor firing rate decreases, and the firing rate through the sinus node and vagal afferents is reduced. The response to a decrease in arterial pressure is described as follows

Increased Sympathetic Nervous System Activity. The primary result is an increase in total vascular resistance. This response is relatively slow (5 to 15 seconds). A small increase in stroke volume secondary to b₁ stimulation and increased contractility also occurs. The increase in vascular resistance is the primary mechanism for restoring blood pressure because an increase in heart rate is relatively ineffective in raising cardiac output. As previously described, if the cardiac output increases without an increase in peripheral vascular tone, the central venous pressure decreases.

The sympathetic nervous system–mediated vasoconstriction decreases blood flow to the splanchnic region, thereby causing a passive release of blood volume from its capacious veins. Visceral organs can transfer as much as 300 to 500 mL of blood into the central circulation.

The importance of vasoconstriction, particularly that involving the splanchnic region, is demonstrated by people with peripheral neuropathy (diabetes mellitus, Parkinson's disease) or spinal cord injury who have severe orthostatic intolerance because of an inability to constrict arterioles in the dependent regions.

Decreased Vagal Activity Resulting in an Increase in Heart Rate. The increase in heart rate is not a primary compensatory response to a decrease in blood pressure. As described by the cardiac output–central venous pressure relation, an increase in heart rate–induced central venous pressure is of limited efficacy in increasing the cardiac output.

ARTERIAL BARORECEPTOR RESPONSE TO INCREASED ARTERIAL PRESSURE

An acute increase in blood pressure results in increased stimulation of the sinoaortic baroreceptors. The increased baroreceptor firing rate increases sinus and vagal afferent input into the nucleus tractus solitarius of the medulla. In response to the increased baroreceptor input, the following occur

1. A rapid (within one beat) decrease in heart rate, secondary to a sudden increase in vagal tone
2. A secondary decrease in stroke volume due to the negative inotropic effects of the increased vagal tone (minor effect)
3. A sympathetic nervous system–mediated decrease in vascular tone (minor effect)

The net result is a decrease in heart rate, with a subsequent decrease in cardiac output and blood pressure. The most important point is that the response, which occurs within one beat, is mediated by a vagally induced decrease in heart rate and cardiac output. The rapid response is extremely important in the protection of the cerebral vessels. Passive vasodilation due to a decrease in sympathetic tone occurs only in the skeletal muscles, and thus cannot contribute greatly to the sudden lowering of arterial blood pressure.

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