Nitric oxide modulates captopril-mediated angiotensin-converting enzyme inhibition in porcine iliac arteries

The influence of the angiotensin-converting enzyme inhibitor captopril on b radykinin-and angiotensin I-induced responses with special regard to nitric oxide (NO) was studied. Auxometric tension and angiotensin-converting enzy me activity was studied in isolated porcine iliac arteries. Captopril poten tiated bradykinin-induced contraction of preparations with intact endotheli um; this potentiation was not seen with the kininase I inhibitor mergepta o r a bradykinin B-1-receptor antagonist. Captopril did not affect bradykinin -induced relaxation. The captopril-mediated increase of bradykinin-induced contraction was only seen in preparations with intact endothelium, while ca ptopril did not affect arterial strips treated with N omega-nitro-L-arginin e. Angiotensin I-induced contractions was less reduced by captopril when th e strips were pretreated with N omega-nitro-L-arginine. Both captopril and the NO donor S-nitroso-N-acetyl-penicillamine inhibited angiotensin-convert ing enzyme activity. An additional reduction in angiotensin-converting enzy me activity was seen when S-nitroso-N-acetyl-penicillamine was added to cap topril-treated preparations. In conclusion, captopril increased bradykinin- induced contraction in a NO-dependent manner. This potentiation is probably mediated by the increased metabolism of bradykinin by kininase I, and the additive angiotensin-converting enzyme inhibitory effect of captopril and N O. (C) 1999 Elsevier Science B.V. All rights reserved.