Mechanism of captopril-induced renal vasodilatation in anesthetized dogs after nonhypotensive hemorrhage.

The roles of renin-angiotensin system and renal prostaglandins (PGs) in mediating the renal vasodilator response of captopril were studied in anesthetized nonhypotensive hemorrhaged dogs. Captopril administered i.v. at a dose of 0.5 mg/kg consistently increased renal blood flow (RBF) and decreased renal vascular resistance. Renal venous PGE concentration and PGE secretion rate were not changed significantly by captopril. In eight dogs, saralasin was infused continuously i.a. to the kidney for the entire experiment. Hemorrhage increased RBF and decreased blood pressure significantly in these animals. Captopril did not further increase RBF in the saralasin-treated kidney and still decreased blood pressure significantly. In hemorrhaged dogs given indomethacin, captopril increased RBF and decreased blood pressure to a similar degree as obtained in the untreated hemorrhaged dogs. These results suggest that under the conditions of these experiments the renal vasodilator effect of captopril is due to the blockade of the renin-angiotensin system and is not associated with either renal PGE release or PG-induced vasodilatation.