ROLE OF KININS IN THE RENAL RESPONSE TO ENALAPRILAT IN NORMOTENSIVE AND HYPERTENSIVE RATS

This study examined the role of endogenous kinins in the alteration of renal hemodynamics induced by low-dose converting enzyme inhibition i n hydropenic normotensive rats and in the nonclipped kidney of hydrope nic two-kidney, one clip hypertensive rats. Infusion of a bradykinin B -2 receptor antagonist (D-Arg(0),[Hyp(3),Thi(5,8),D-Phe(7)]-bradykinin , 1 or 10 mu g . kg(-1). min(-1)) did not alter renal function of norm otensive rats. In a second series of experiments, infusion of enalapri lat at 0.1 mg . kg(-1). h(-1) increased renal blood flow (P<.01) and d ecreased renal vascular resistance (P<.01). The superimposition of the kinin antagonist at 1 mu g . kg(-1). min(-1) during the enalaprilat i nfusion decreased renal blood flow to a value similar to the preenalap rilat baseline and significantly different from the mean of the two en alaprilat periods before and after the addition of the kinin antagonis t-the ''mean effect of enalaprilat.'' The decrease in renal blood flow induced by the kinin antagonist was associated with an increase in re nal vascular resistance above the mean effect of enalaprilat (P<.025). In two-kidney, one clip hypertensive rats, systemic infusion of enala prilat augmented the hemodynamics of the nonclipped kidney by a degree similar to that in normotensive rats. In contrast to normotensive rat s, superimposition of the kinin antagonist did not alter the enalapril at-induced change in blood flow or vascular resistance of the nonclipp ed kidney. The results of this study suggest that endogenous kinins co ntribute to the increased renal function induced by low-dose convertin g enzyme inhibition in hydropenic normotensive rats but appear to cont ribute less to the enalaprilat-induced alterations of renal function i n the nonclipped kidney of two-kidney, one clip hypertensive rats.