Abstract

The baroreceptor reflex is a relatively high gain control system that maintains arterial pressure within normal limits. To a large extent, this is accomplished through central neural pathways responsible for autonomic outflow residing in the medulla oblongata. The circulating renin-angiotensin system also contributes to the regulation of blood pressure, predominantly through its effects on the control of hydromineral balance and fluid volume. All the components of the renin-angiotensin system are also found in the brain. One of the principal products of the renin-angiotensin system cascade (brain or blood), angiotensin II, modulates the baroreceptor reflex by diminishing the sensitivity of the reflex and shifting the operating point for regulation of sympathetic outflow to higher blood pressures. This paper reviews our current knowledge about the neuronal pathways in the medulla oblongata through which angiotensin peptides alter the baroreceptor reflex control of sympathetic nerve activity. Emphasis is placed on the probable components and neural mechanisms of the medullary baroreflex arc that account for the ability of angiotensin peptides to change the sensitivity of the baroreceptor reflex and to shift the baroreceptor reflex control of sympathetic outflow to higher blood pressures in a pressure-independent manner.

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