Adrenal responsiveness to
angiotensin II (AII) and the diastolic blood pressure responses to
saralasin were studied in 19 patients with high
renin essential hypertension (HREH) on a 10-meq Na(+)/100 meq K(+) diet. The increment in plasma
renin activity (PRA) between supine and upright positions was used as an estimate of the acute stimulation of the adrenal gland by endogenous AII; the normal increment in plasma
aldosterone divided by the increment in PRA was >3.8. 7 of 19 had abnormal upright posture responses with significantly greater mean PRA increments (24+/-6 ng/ml per h) and significantly smaller plasma
aldosterone increments 47 +/- 16 ng/dl) (P < 0.036) compared to the increments observed in HREH patients with normal adrenal responsiveness (PRA = 15 +/- 1 ng/ml per h; plasma
aldosterone = 87 +/- 17 ng/dl). When AII was infused at doses of 0.1-3 ng/kg per min, only patients with normal posture responses had normal plasma
aldosterone increments; plasma
aldosterone levels failed to significantly increase even at the highest infusion rate in the patients with the abnormal upright posture responses. The AII competitive inhibitor,
saralasin (0.3-30 mug/kg per min) was then infused to study the occurrence of angiotensinogenic
hypertension in both HREH subgroups. The mean decline in diastolic blood pressure to
saralasin in the subnormal adrenal responsive patients (-15 +/- 3 mm Hg) was significantly greater than in the normal adrenal responsive group (-3 +/- 2 mm Hg) (P < 0.02).It is concluded that patients with HREH are not a homogeneous population; approximately one-third have AII-dependent
hypertension. In these patients, the mechanism responsible for the elevated
renin and blood pressure could be a compensatory increase secondary to decreased adrenal responsiveness to AII. In the remainder, the high PRA levels have little, if any, causal role in the pathogenesis of the
hypertension but could reflect a marker of other pathophysiologic processes.