Hypotensive effect of captopril and decreased rat uterine bradykinin receptors.

Abstract

To determine the role of local bradykinin at the level of the vascular smooth muscle receptors in the hypotensive effect of captopril, we assessed the effects of prolonged intravenous infusions for up to 7 days of bradykinin (0.1 microgram/min) and captopril (1.7 micrograms/min) on systolic blood pressure and uterine bradykinin receptors in normotensive rats. Bradykinin infusion was associated with a transient fall in systolic blood pressure at Day 1 (117.5 +/- 2.8 mmHg vs. 125.8 +/- 1.7, p less than 0.05) and returned to control levels by Day 3. Following captopril infusion there was a similar but more persistent fall in systolic blood pressure (115.3 +/- 2.4 mmHg vs. 125.8 +/- 1.7, p less than 0.01 at Day 1 and 111.0 +/- 2.4 mmHg vs. 125.0 +/- 1.9, p less than 0.001 at Day7). After 2 days of bradykinin infusion the number of bradykinin receptors was decreased (39.9 +/- 2.1 fmol/mg protein vs. 49. 9 +/- 2.4, p less than 0.01) and returned to controls at Day 7, while captopril infusion induced a prolonged decrease (42.3 +/- 1.8 fmol/mg protein vs. 49.9 +/- 2.4, p less than 0.05 at Day 2 and 38.8 +/- 2.4 fmol/mg protein vs. 44.5 +/- 1.3, p less than 0.05 at Day 7). Present results suggest that the increased vascular tissue level of bradykinin can contribute directly to the acute hypotensive effect of captopril. However, it may play only a minor role for the chronic hypotensive effect of captopril.