Effect of infused captopril on blood pressure and the renin-angiotensin-aldosterone system in normal dogs subjected to varying sodium balance

Infusion of captopril at 20, 200, 2,000 and 6,000 μg/kg/hour into sodium-depleted conscious dogs produced a rapid, dose-dependent decrease in blood pressure and plasma angiotensin II and III, maximal suppression being achieved at 200 μg/kg/hour (97 ± 14 to 65 ± 8 [standard deviation]mm Hg, 38 ± 10.6 to 3.2 ± 1.5 pmol/liter and 7.0 ± 4.8 to 1 ± 0.5 pmol/liter, respectively). Angiotensin I concentration increased with each infusion rate to a maximal 16-fold increase at 6,000 μg/kg/hour (26 to 416 pmol/liter). For all infusion rates the percentage decrease in blood pressure correlated with the percentage decrease in plasma angiotensin II (r = 0.65, p < 0.001). Infusion of captopril at 6,000 μg/kg/hour into sodium-loaded dogs also produced a decrease in both blood pressure (117 ± 9 to 96.6 ± 11 mm Hg) and plasma angiotension II (11.0 ± 3 to 1.6 ± 1.3 pmol/liter). Plasma aldosterone concentrations decreased whereas both blood angiotensin I and renin concentration increased. In another experiment angiotensin II was infused at 2, 6, 18 and 54 ng/kg/min into sodium-depleted dogs firstly without modification and secondly combined with captopril (6,000 μg/kg/hour) given for 1 hour before the angiotensin dose-response study and continued throughout. Angiotensin II infusion raised mean arterial pressure and plasma angiotensin II in each animal. However, the angiotensin II blood pressure dose-response curve was shifted downwards and to the right in the captopril-treated animals.These results suggest that arterial pressure and aldosterone secretion in normal dogs are partly dependent on the renin-angiotensin system but that not all of the acute decrease in blood pressure produced by captopril can be explained by the suppression of the acute vasoconstrictor effect of circulating angiotensin II.