Role of kinins in the acute antihypertensive effect of the converting enzyme inhibitor, captopril.

Abstract

The role of kinins in the acute antihypertensive effect of a converting enzyme inhibitor (CEI) was studied in sodium-depleted normotensive and in two-kidney, one clip chronically hypertensive rats (2K-1C). The 2K-1C were on a normal sodium diet. The acute vasodepressor effect of the CEI was determined in these two groups either after administration of normal rabbit globulins or antikinin globulins. The amount of kinin antibodies administered completely blocked the hypotensive effects of bradykinin, 400 ng/kg, and urinary kallikrein, 4 microgram/kg. After administration of CEI in the sodium-depleted rats there was no significant difference (p greater than 0.05) in the acute changes in mean blood pressure (BP) between the group pretreated with normal rabbit globulins (delta BP -32.3 +/- 3.9 mm Hg) and the group pretreated with antikinin globulins (delta BP -25 +/- 2.5 mm Hg). In the 2K-1C pretreated with normal rabbit globulins, the CEI produced a decrease in BP of -21 +/- 4.5 mm Hg. This decrease was almost completely blocked in the group pretreated with the antikinin globulins (delta BP -4 +/- 4.1 mm Hg). These differences in the changes in BP were significant (p less than 0.02). These results suggest that the acute antihypertensive effect of the CEI in the sodium-depleted rats is probably due to inhibition of the conversion of angiotensin I to II while in the 2K-1C it is due, in part, to an increase in kinin concentrations secondary to the inhibition of kininase II.