A primary role for vasopressin in the genesis of essential hypertension.

Abstract

Alterations in the renin-angiotensin system are caused by changes in the vascular perfusing pressures in the renal outer cortex. The renal peripheral resistance to the perfusing pressures in the renal outer cortex is to some extent controlled by the plasma sodium load, sympathetic, and vasoconstrictor stimuli. Logically, therefore, the renin-angiotensin system can be excluded from any primary involvement in the genesis of essential hypertension. Because high plasma renin hypertension inevitably progresses to organic vascular involvement, it is clear that angiotensin-ii plays an important vasoconstrictor role at some later stage. Experiments, involving Goldblatt techniques, which alter the renal perfusion pressure and hence activate the renin-angiotensin system, skip over a preliminary period during which, under natural conditions, unknown factors are slowly inducing an increase in the total peripheral resistance. It is argued that the dominant natural factor during this preliminary period is an excess general vasotonic influence exerted by vasopressin.It is argued that essential hypertension develops in those individuals who, for some reason, over a long period of time intermittently release excessive amounts of vasopressin and who also possess a particularly hyper-reactive renal-adrenal feed-back system. Built into this system is the capability of activating a catecholamine overdrive postulated by several authors as an important, though secondary factor, in the development of essential hypertension.