Effect of angiotensin III on blood pressure, renin-angiotensin-aldosterone system in normal and hypertensive subjects.

The biological actions of angiotensin III (AIII) in animals have been reported to be stimulation of aldosterone secretion and vasoconstriction. However, the biological actions of AIII in human essential hypertension (EH) have not been evaluated. Twenty ng/Kg/min of AIII was infused intravenously for 30 min into 6 normal subjects and 24 patients with EH. The systolic blood pressure was elevated significantly, from 116 +/- 5 (mean +/- SD)/68 +/- 4 to 137 +/- 9/74 +/- 5 mmHg in normal subjects and from 155 +/- 29/95 +/- 17 to 176 +/- 26/106 +/- 20 mmHg in EH patients. The elevation in systolic BP of low-renin EH patients was significantly larger than that of normal-renin EH patients. Plasma renin activity (PRA) decreased significantly from 1.64 +/- 1.07 to 1.21 +/- 1.05 ng/ml/hr in normal subjects and from 0.88 +/- 0.66 to 0.76 +/- 0.63 ng/ml/hr in EH. Plasma aldosterone concentration (PAC) increased significantly from 57 +/- 34 to 116 +/- 34 pg/ml in normal subjects and from 66 +/- 56 to 91 +/- 24 pg/ml/ in EH. There was no significant difference between the increase of PAC in low-renin EH and in normal-renin EH. Plasma cortisol concentration (PCC) did not change in these subjects. There were no significant relationships between the changes of PRA and PAC or PRA and blood pressure. These results suggest that the pressor action of AIII appeared in relation to the basal PRA in EH. In EH, PRA is suppressed by the direct action of AIII in the kidney and neither by increased PAC nor by increased blood pressure. The small changes in blood pressure caused by AII infusion suggest that a test using an AIII infusion for aldosterone stimulation would be preferable to an angiotensin II infusion.