Relationship between the circulating and vascular renin-angiotensin systemand the vasodilating effect of captopril in human hypertension

A vascular renin-angiotensin system (RAS) is present in the forearm vascula ture of essential hypertensive patients and is closely related to the circu lating renin profile. To test whether the haemodynamic effect of acute intr abrachial administration of captopril is related to the circulating and/or vascular RAS, 31 hypertensive patients were selected and divided into four groups according to their different circulating RAS profile (n = 7 hyperten sive patients with primary aldosteronism and suppressed plasma renin activi ty; n = 7 low renin essential hypertensive patients; n = 8 normal renin ess ential hypertensive patients; n = 9 high renin renovascular hypertensive pa tients). The forearm net balance of active renin, plasma renin activity and angiotensin II, obtained by intrabrachial infusion of the P-adrenergic rec eptor agonist isoproterenol (0.03, 0.1, 0.3 mu g/100 ml/min) and calculated as the product of the venous-arterial plasma concentration gradient and fo rearm blood flow (FBF), was closely related to the circulating RAS. Captopr il (0.25, 2.5, 25 mu g/100 ml/min per 20 min each dose) unchanged basal FBF in the primary aldosteronism and low renin groups (FBF increase: from 3.9 +/- 0.4 to a maximum of 4.1 +/- 0.5 and from 3.8 +/- 0.3 to a maximum of 4. 3 +/- 0.5 ml/100 ml/min, respectively), whereas it caused slight vasodilati on in the normal renin group (from 3.9 +/- 0.3 to a maximum of 5.3 +/- 0.7 ml/100 ml/min), and pronounced vasodilation in the high renin group (from 4 .0 +/- 0.4 to a maximum of 6.4 +/- 0.5 ml/100 ml/min). Captopril-induced va sodilation showed a significant direct correlation with the circulating and vascular RAS. The present data, while confirming the existence of a vascul ar RAS in the forearm of hypertensive patients indicate that the acute vaso dilating effect of intrabrachial captopril is linked to a stimulated RAS, e ither circulating or vascular, supporting the evidence that, in acute condi tions, ACE inhibitors exert their vasodilating effect through the RAS block ade.