Interaction between renin and the autonomic nervous system in hypertension

Abstract

The abnormal distribution of plasma renin values described in established essential hypertension are also found in patients with very early, borderline hypertension. In established hypertension, renin values have been used to draw inferences about the pathophysiology of blood pressure elevation. Within this concept, the low-renin state is considered a volume-dependent (volume expanded) form of hypertension. The high-renin state is viewed as high-resistance hypertension caused by a renin-dependent vasoconstriction. However, the pathophysiology of high- and low-renin borderline hypertension does not follow the prediction from the volume-vasoconstriction theory. The high-renin state is often associated with an increase in cardiac output and normal values of vascular resistance. Even when the cardiac output is normal and the total peripheral resistance is elevated in high renin, the vasoconstriction is not renin-angiotensin dependent. The high-renin borderline and mild hypertension is a state of generalized, increased, sympathetic drive to the heart, blood vessels, and kidneys. After the influence of the autonomic nervous system is removed by pharmacologic blockade, blood pressure in patients with high-renin values becomes normal. To the contrary, pharmacologic antagonization of angiotensin II with a converting enzyme inhibitor does not lead to normal blood pressure values in patients with high-renin. Patients with borderline hypertension with low renin have normal plasma and blood volume values. However, because of decreased compliance of the peripheral capacitance space, the blood volume is shifted from the peripheral to the central (cardiopulmonary) portion of the circulation. Expansion of the cardiopulmonary blood volume causes a larger stretch of cardiopulmonary mechanoreceptors, which, in turn, elicits a preferential inhibition of the sympathetic tone to the kidneys. The low-renin and low sympathetic tone in these patients are the consequence of the expansion of the cardiopulmonary blood volume and not of the total blood volume.