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.