On Renin Substrate and Hypertension

Abstract

In essential hypertension, the renin angiotensin system as measured in the peripheral circulating blood has failed to qualify as one of the contenders for a primary ‘fault’ in hypertension. The question is ably discussed by Professor John Swales in this volume. Renin, the proteolytic enzyme responsible for generating the vasoactive angiotensin from angiotensinogen, has been traditionally regarded as the driving force for the entire system. In untreated patients with essential hypertension, measurements of plasma renin activity correlate well with measured levels of the active end product of the system; e.g., angiotensin II. The same is true if renin release is acutely stimulated or suppressed. Under most conditions, the activity of the renin angiotensin system in the periphery is presumably altered by changing the amount the enzyme renin released, as the levels of angiotensinogen in plasma are not altered, either, in essential hypertension or during acute stimulatory or suppressive responses of renin release. Furthermore, there is no good available evidence (Swales, this volume) that the activity of the peripheral renin angiotensin system in essential hypertension is dictated by an inappropriate metabolic fate or altered sensitivity to the generated angiotensin at the receptor sites on the blood vessels.