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(Hypertension. 1996;27:235-244.)
© 1996 American Heart Association, Inc.

Articles

Role of Kinins in the Renal Response to Enalaprilat in Normotensive and Hypertensive Rats

Presented in part at the Southern and National Meetings of the American Federation of Clinical Research, New Orleans, La, January, 1990, and Washington, DC, May, 1990, and the American Society of Nephrology, Baltimore, Md, November, 1991, and published in abstract form (Clin Res. 1990;38:21A, Clin Res. 1990;38:428A, and J Am Soc Nephrol. 1991;2:475).

Wayne R. Fitzgibbon; Ayad A. Jaffa; Ronald K. Mayfield; David W. Ploth

From the Divisions of Nephrology (W.R.F., D.W.P.) and Endocrinology (R.K.M.), Department of Medicine and Department of Pharmacology (A.A.J.), Medical University of South Carolina, Charleston, and the Ralph H. Johnson Veterans Affairs Medical Center (D.W.P., R.K.M.).

Correspondence to David W. Ploth, MD, Division of Nephrology, Department of Medicine, Medical University of South Carolina, 171 Ashley Ave, Charleston, SC 29425-2220.

Abstract This study examined the role of endogenous kinins in the alteration of renal hemodynamics induced by low-dose converting enzyme inhibition in hydropenic normotensive rats and in the nonclipped kidney of hydropenic two-kidney, one clip hypertensive rats. Infusion of a bradykinin B₂ receptor antagonist (D-Arg⁰,[Hyp³,Thi^5,8,D-Phe⁷]-bradykinin, 1 or 10 µg · kg^-1 · min^-1) did not alter renal function of normotensive rats. In a second series of experiments, infusion of enalaprilat at 0.1 mg · kg^-1 · h^-1 increased renal blood flow (P<.01) and decreased renal vascular resistance (P<.01). The superimposition of the kinin antagonist at 1 µg · kg^-1 · min^-1 during the enalaprilat infusion decreased renal blood flow to a value similar to the preenalaprilat baseline and significantly different from the mean of the two enalaprilat periods before and after the addition of the kinin antagonist—the "mean effect of enalaprilat." The decrease in renal blood flow induced by the kinin antagonist was associated with an increase in renal vascular resistance above the mean effect of enalaprilat (P<.025). In two-kidney, one clip hypertensive rats, systemic infusion of enalaprilat augmented the hemodynamics of the nonclipped kidney by a degree similar to that in normotensive rats. In contrast to normotensive rats, superimposition of the kinin antagonist did not alter the enalaprilat-induced change in blood flow or vascular resistance of the nonclipped kidney. The results of this study suggest that endogenous kinins contribute to the increased renal function induced by low-dose converting enzyme inhibition in hydropenic normotensive rats but appear to contribute less to the enalaprilat-induced alterations of renal function in the nonclipped kidney of two-kidney, one clip hypertensive rats.

Key Words: angiotensin-converting enzyme inhibitors • bradykinin • enalapril • hypertension, renovascular • kinins • vasodilation

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