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European Heart Journal 1993 14(1):106-112;
Copyright © 1993 by the European Society of Cardiology.
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© 1993 The European Society of Cardiology

Deleterious effect of exogenous angiotensin-I on the extent of regional ischaemia and its inhibition by captopril

A. F. E. RUMP, T. J. RÖSEN, A. KORTH and W. KLAUS

Institut für Pharmakologie Universität Köln Germany

Received 27 August 1991; revised 8 June 1992; .

Correspondence: A. F E Rump, Institui für Pharmakologie, Universität zu Köln. Gleuclersiraße 24, D-5000 Köln 41, Germany

Abstract

The endogenous activity of the local renin-angiotensin system (RAS) and the anti-ischaemic properties of captopril were investigated in electrically driven rabbit Langendorff hearts (constant pressure: 70 cmH2O, Tyrode solution, Ca2+ 1.8 mmol.l–1). Cumulative concentration-response curves showed no significant difference (P>0.05) between the reduction of the global coronary flow (CF) by exogenous angiotensin-I or angiotensin-II (EC50 = 10–10 mol.l–1). It is concluded that the local RAS in isolated rabbit hearts is highly sensitive, whereas its endogenous activity is very low due to very low endogenous angiotensin-I content. Myocardial ischaemia (MI) was induced by the occlusion of a left coronary artery branch and MI was quantified from NADH surface fluorescence photography. MI was significantly enlarged (+35%) (P <0.05) by exogenous angiotensin-I (6x10–9 mol.l–1). The reduction in CF and the increment in MI by angiotensin-I could be completely prevented by adding captopril at a low concentration (10–6 mol.l–1) to the perfusion buffer. In the absence of exogenous angiotensin-I, captopril alone (10–6 mol.l–1) neither significantly enhanced CF (P >0.05), nor diminished MI (P >0.05), supporting the finding of very low endogenous activity of tile local RAS in this model. We, moreover, conclude that at a low concentration (10–6 mol.l–1) captopril does not possess direct cardioprotective properties independent of its ACE inhibiting action.

Key Words: NADH fluorescence • angiotensin • angiotensin-converting enzyme • myocardial ischaemia • ACE inhibitors • captopril • cardioprotection


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