Aldosterone Response to Long Term Infusion of Angiotensin II and Angiotensin III in Conscious Dogs before and after Dietary Sodium Restriction*

The aldosterone and arterial blood pressure response to long term infusion of angiotensin II (AII) and (des-asp1)-angiotensin II (A-III) was studied in conscious dogs before and after dietary sodium restriction. Plasma aldosterone concentration (PAC), plasma cortisol concentration (PCC), and plasma renin activity (PRA) were determined by RIA. During long term infusion of A-II (15 ng/kg min-1) in sodium-replete animals, PAC increased from 7.1 ± 2.9 ng/100 ml to a steady state level of 14.7 ± 4.6 ng/100 ml (mean ± SE; P < 0.01), PRA was undetectable by RIA, and arterial pressure increased from 103 ± 5 to 142 ± 8 mm Hg (P < 0.001). During long term infusion of A-III (30 ng/kg min-1) in sodium-replete animals, PAC increased from 8.3 ± 3.4 ng/100 ml to a steady state level of 15.9 ± 5.2 ng/100 ml (P < 0.01), PRA decreased from 0.79 ± 0.21 to 0.61 ± 0.32 ng/ml/h (NS, P > 0.05), and arterial pressure failed to change from control levels of 103 ± 5 mm Hg. During long term infusion of A-II (15 ng/kg min-1) in sodium-deplete animals, PAC increased from 36.3 ± 10.4 ng/100 ml to a steady state level of 94.3 ± 17.8 ng/100 ml (P < 0.01), while PRA and arterial pressure remained near control levels. During long term infusion of A-III (30 ng/kg min-1) in sodium-deplete animals, PAC increased from 39.1 ± 9.8 ng/100 ml to a steady state level of 79.9 ± 16.7 ng/100 ml (P < 0.01), while PRA and arterial pressure remained near control levels. These data demonstrate that the adrenal glomerulosa response to angiotensin II and (des-asp1)-angiotensin II is markedly increased during sodium deficiency and support the concept that increased aldosterone biosynthesis during sodium deficiency is mediated in part by increased activity of the renin-angiotensin system.