Nitric oxide modulates captopril-mediated angiotensin-converting enzyme inhibition in porcine iliac arteries
1999 (English)In: European Journal of Pharmacology, ISSN 0014-2999, E-ISSN 1879-0712, Vol. 385, no 1, 21-27 p.Article in journal (Refereed) Published
The influence of the angiotensin-converting enzyme inhibitor captopril on bradykinin-and angiotensin I-induced responses with special regard to nitric oxide (NO) was studied. Auxometric tension and angiotensin-converting enzyme activity was studied in isolated porcine iliac arteries. Captopril potentiated bradykinin-induced contraction of preparations with intact endothelium; this potentiation was not seen with the kininase I inhibitor mergepta or a bradykinin B1-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 captopril did not affect arterial strips treated with Nω-nitro-L-arginine. Angiotensin I-induced contractions was less reduced by captopril when the strips were pretreated with Nω-nitro-L-arginine. Both captopril and the NO donor S-nitroso-N-acetyl-penicillamine inhibited angiotensin-converting enzyme activity. An additional reduction in angiotensin-converting enzyme activity was seen when S-nitroso-N-acetyl-penicillamine was added to captopril-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 NO.
Place, publisher, year, edition, pages
Elsevier, 1999. Vol. 385, no 1, 21-27 p.
Angiotensin-converting enzyme activity, Bradykinin, Captopril, Contraction, Nitric oxide (NO), Relaxation
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:liu:diva-79492DOI: 10.1016/S0014-2999(99)00689-5OAI: oai:DiVA.org:liu-79492DiVA: diva2:543037