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Am J Physiol Heart Circ Physiol 270: H1985-H1992, 1996;
0363-6135/96 $5.00
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AJP - Heart and Circulatory Physiology, Vol 270, Issue 6 1985-H1992, Copyright © 1996 by American Physiological Society

ARTICLES

Bradykinin pathway is involved in acute hemodynamic effects of enalaprilat in dogs with heart failure

F. Barbe, J. B. Su, T. T. Guyene, B. Crozatier, J. Menard and L. Hittinger
Institut National de la sante et de la Recherche Medicale, Faculte de Medecine, Creteil, France.

To determine the role of the renin-angiotensin system and the bradykinin pathway in the mechanism of action of angiotensin-converting enzyme inhibitors in heart failure, the acute effects of enalaprilat (1 mg/kg) were compared with those of a renin inhibitor (ciprokiren, 1 mg/kg i.v.) in 10 chronically instrumented conscious dogs with heart failure induced by right ventricular pacing (3 wk, 240 beats/min). The effects of enalaprilat and ciprokiren on bradykinin infusion (3, 10, and 30 micrograms/min) and the effects of enalaprilat in the presence of the bradykinin B2 receptor antagonist Hoe-140 (10 micrograms/kg i.v.) were also examined. Both inhibitors significantly decreased mean aortic pressure and increased cardiac output. However, enalaprilat induced significantly greater hemodynamic effects than ciprokiren (mean aortic pressure, -13 +/- 3 vs. -6 +/- 1 mmHg; cardiac output, 0.4 +/- 0.1 vs. 0.15 +/- 0.1 l/min). Bradykinin infusion led to dose-dependent decreases in mean aortic pressure and increases in cardiac output that were not modified by pretreatment with ciprokiren but were potentiated 10-fold by enalaprilat. Hoe-140 significantly reduced the hemodynamic effects of enalaprilat. Thus endogenous bradykinin is involved in the acute hemodynamic effects of enalaprilat in experimental heart failure.


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