This Article Full Text 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 Jover, B. Articles by Mimran, A. Search for Related Content PubMed PubMed Citation Articles by Jover, B. Articles by Mimran, A.

(Hypertension. 1996;27:79-84.)
© 1996 American Heart Association, Inc.

Articles

Chronic Kinin Blockade and Effect of Ramipril in Renal Adaptation to Sodium Restriction

Bernard Jover; Abderraouf Hérizi; Albert Mimran

From Groupe Rein et Hypertension, Centre Hospitalier Universitaire, Montpellier, France.

Correspondence to Bernard Jover, Groupe Rein et Hypertension, Centre Hospitalier Universitaire, Hôpital St Charles, 34 295 Montpellier Cedex 5, France.

Abstract The contribution of endogenous kinins to impairment in renal adaptation to a 6-day period of dietary sodium withdrawal associated with treatment with ramipril (5 mg/kg per day) and losartan (30 mg/kg per day) was evaluated by use of concomitant chronic administration of the bradykinin B₂-receptor antagonist Hoe 140 (150 or 300 µg/kg per day via subcutaneous osmotic pump). A similar level of higher cumulative sodium excretion was observed in ramipril- and losartan-treated rats compared with untreated animals, and the effect of ramipril was not affected by Hoe 140. Similarly, the fall in arterial pressure and the renal vasodilatation associated with ramipril and losartan were not modified by Hoe 140. Glomerular filtration rate (785±73 µL/min per g KW in untreated sodium-depleted rats) decreased to a larger extent in ramipril-treated rats compared with losartan-treated rats (371±78 and 550±55 µL/min per g KW, respectively). Hoe 140 markedly prevented the alteration in glomerular filtration rate associated with ramipril, thus resulting in a final glomerular filtration rate (543±41 µL/min per g KW) similar to that observed with losartan. These findings demonstrate that despite a lack of influence on arterial pressure and sodium balance, accumulation of kinins markedly contributes to deterioration of the glomerular filtration rate induced by ramipril in sodium-depleted rats.

Key Words: renal circulation • receptors, angiotensin • angiotensin-converting enzyme inhibitors • bradykinin

This article has been cited by other articles:

				S. Kim, Y. Zhan, Y. Izumi, and H. Iwao Cardiovascular Effects of Combination of Perindopril, Candesartan, and Amlodipine in Hypertensive Rats Hypertension, March 1, 2000; 35(3): 769 - 774. [Abstract] [Full Text] [PDF]

				R. Willenbrock, M. Scheuermann, G. Thibault, Markus Haass, K. Hohnel, J. Bohlender, F. C. Luft, and Rainer Dietz Angiotensin inhibition and atrial natriuretic peptide release after acute volume expansion in rats with aortocaval shunt Cardiovasc Res, June 1, 1999; 42(3): 733 - 742. [Abstract] [Full Text] [PDF]

				R. WILLENBROCK, I. PAGEL, M. SCHEUERMANN, K. HÖHNEL, H. S. MACKENZIE, B. M. BRENNER, and R. DIETZ Renal Function in High-Output Heart Failure in Rats: Role ofEndogenous Natriuretic Peptides J. Am. Soc. Nephrol., March 1, 1999; 10(3): 572 - 580. [Abstract] [Full Text]

				J. L. Pasquie, A. Herizi, B. Jover, and A. Mimran Chronic Bradykinin Infusion and Receptor Blockade in Angiotensin II Hypertension in Rats Hypertension, March 1, 1999; 33(3): 830 - 834. [Abstract] [Full Text] [PDF]