Effect of des-Asp1-Angiotensin II on Secretion and Metabolism of Aldosterone*

Angiotensin III (AIII; des-Asp1-AII) was infused into 13 sodium-deplete, dexamethasone-pretreated normal men at rates of 2–20 ng/kg • min. Each rate of infusion was maintained for 20–30 min. The MCR of aldosterone was determined by constant infusion of [3H]aldosterone. Plasma concentrations of endogenous and labeled steroids were measured simultaneously. The plasma aldosterone concentration (PAC) increased from 31 ± 4 (mean ± SEM) to 34 ± 5, 40 ± 8, 48 ± 7, and 63 ± 22 ng/dl when AIII was infused at 2, 4, 8, and 12 ng/kg-min. There was wide variation in the individual PAC responses to AIII infusion. The threshold for the AHI-stimulated rise in PAC was less than or equal to 2 ng/kg-min in 10 subjects. In the other 3 subjects, the threshold was between 4–8 ng/kg-min. The MCR of plasma aldosterone decreased from 910 ± 33 to 832 ± 36 ml/min, and the whole blood MCR decreased from 1312 ± 71 to 1114 ± 69 ml⁄min during AIII infusion. The decline in MCR contributes less than 15% to the observed rise in PAC, the largest part of the increase being due to higher secretion rate. Plasma cortisol and deoxycorticosterone concentrations were not significantly increased. PRA declined from 2.69 ± 0.29 to 2.13 ± 0.34 ng/ml-h, but inactive renin in plasma did not change. Systolic blood pressure rose from 121 ± 2 to 131 ± 1 mm Hg at 16 ng/kg-min; diastolic blood pressure was unchanged. AIII is an effective stimulus for aldosterone secretion in sodiumdeplete men.