This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Hajj-ali, A. F. Articles by Zimmerman, B. G. Search for Related Content PubMed PubMed Citation Articles by Hajj-ali, A. F. Articles by Zimmerman, B. G.

Hypertension, Vol 17, 504-509, Copyright © 1991 by American Heart Association

ARTICLES

Kinin contribution to renal vasodilator effect of captopril in rabbit

AF Hajj-ali and BG Zimmerman
Department of Pharmacology, University of Minnesota, Minneapolis 55455.

This study was conducted to examine the role of bradykinin in the persistence of the renal vasodilator effect of captopril during angiotensin II receptor blockade. Blood pressure and renal blood flow were monitored in eight groups of pentobarbital-anesthetized rabbits. In group 4, captopril alone was administered, and it decreased blood pressure by 14 +/- 4 mm Hg and increased renal blood flow by 21 +/- 4 ml/min. After a bolus injection and a constant intravenous infusion of the imidazole derivative angiotensin II receptor antagonist DuP 753 (group 5), captopril decreased blood pressure by 9 +/- 2 mm Hg and increased renal blood flow by 8 +/- 1 ml/min (12 +/- 1% change in renal blood flow, p less than 0.05 versus group 4). In the presence of a constant intravenous infusion of saralasin (group 6), captopril decreased blood pressure by 13 +/- 5 mm Hg and increased renal blood flow by 7 +/- 2 ml/min (17 +/- 5% change in renal blood flow, p less than 0.05 versus group 4). These results did not differ from those in group 5. During a constant intrarenal arterial infusion of a B2 bradykinin receptor antagonist, DArg0, [Hyp3-Thi5,8-DPhe7]-bradykinin (BkA) (group 7), captopril decreased blood pressure by 14 +/- 4 mm Hg and increased renal blood flow by 10 +/- 4 ml/min. Combined administration of DuP 753 intravenously and BkA intra-arterially (group 8) eliminated the effect of captopril. In group 8, captopril caused insignificant changes in blood pressure and renal blood flow. The results indicate that DuP 753 and saralasin antagonize the renin- angiotensin system to a comparable extent in vivo. Although blockade of the latter system accounted for a significant part of the increase in renal blood flow caused by captopril, the remaining component was contributed by endogenous bradykinin.

This article has been cited by other articles:

				M C. Lansang and N. K Hollenberg ACE inhibition and the kidney: species variation in the mechanisms responsible for the renal haemodynamic response Journal of Renin-Angiotensin-Aldosterone System, June 1, 2000; 1(2): 119 - 124. [PDF]

				N. K. Hollenberg Implications of Species Difference for Clinical Investigation : Studies on the Renin-Angiotensin System Hypertension, January 1, 2000; 35(1): 150 - 154. [Abstract] [Full Text] [PDF]

				H. Yu, O. A. Carretero, L. A. Juncos, and J. L. Garvin Biphasic Effect of Bradykinin on Rabbit Afferent Arterioles Hypertension, August 1, 1998; 32(2): 287 - 292. [Abstract] [Full Text] [PDF]

				N. K. Hollenberg and E. Guidi ACE Inhibitors and Renal Vascular Responses in the Spontaneously Hypertensive Rat Journal of Cardiovascular Pharmacology and Therapeutics, January 1, 1998; 3(2): 161 - 169. [Abstract] [PDF]

				H. Ono, Y. Ono, and E. D. Frohlich ACE Inhibition Prevents and Reverses L-NAMEExacerbated Nephrosclerosis in Spontaneously Hypertensive Rats Hypertension, February 1, 1996; 27(2): 176 - 183. [Abstract] [Full Text]

				W. R. Fitzgibbon, A. A. Jaffa, R. K. Mayfield, and D. W. Ploth Role of Kinins in the Renal Response to Enalaprilat in Normotensive and Hypertensive Rats Hypertension, February 1, 1996; 27(2): 235 - 244. [Abstract] [Full Text]

				N. K. Hollenberg and N. D. L. Fisher Renal Circulation and Blockade of the Renin-Angiotensin System : Is Angiotensin-Converting Enzyme Inhibition the Last Word? Hypertension, October 1, 1995; 26(4): 602 - 609. [Abstract] [Full Text]