Evidence That the Acute Hypotensive Effect of Captopril in Dogs is Not Wholly Explained by a Reduction of Plasma Angiotensin II and its Direct Vasoconstrictor Effect

Abstract

1. Captopril infused into sodium-loaded dogs produced a fall in both blood pressure [117 ± 9.7 to 96.6 ± 11.4 (sd) mmHg] and plasma angiotensin II [11.0 ± 3.0 to 1.6 ± 1.3 (sd) pmol/l]. Plasma aldosterone fell while both blood angiotensin I and renin concentration rose. 2. Angiotensin II was infused at 2, 6, 18 and 54 ng min⁻¹ kg⁻¹ into sodium-depleted dogs. Plasma angiotensin II and arterial pressure both rose and were related in a dose-response curve. 3. On a separate occasion the same dogs were given an intravenous infusion of captopril (6 mg h⁻¹ kg⁻¹) and the angiotensin II infusion was repeated. Again plasma angiotensin II and arterial pressure rose but the dose-response curve was displaced downwards; a higher concentration of angiotensin II being required to produce the same blood pressure as in the dogs not given captopril. 4. These findings suggest that the acute hypotensive effect of captopril is not wholly explained by a decrease in plasma angiotensin II concentration and the consequent reduction of its acute vasoconstrictor effect.