Abstract
The aldosterone and arterial blood pressure response to long term infusion of angiotensin II (A-II) and (des-Asp1)-angiotensin II (A-III) was studied in conscious dogs before and after dietary Na restriction. Plasma aldosterone concentration (PAC), plasma cortisol concentration (PCC), and plasma renin activity (PRA) were determined by RIA [radioimmunoassay]. During long term A-II infusion (15 ng/kg min-1) in Na-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 (300 ng/kg min-1) in Na-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 per h (NS, P > 0.05), and arterial pressure failed to change from control levels of 103 .+-. 5 mm Hg. During long term A-II infusion (15 ng/kg min-1) in Na-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 A-III infusion (30 ng/kg min-1) in Na-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. Adrenal glomerulosa response to A-II and A-III is markedly increased during Na deficiency and support the concept that increased aldosterone biosynthesis during Na deficiency is mediated in part by increased activity of the renin-angiotensin system.