nitroarginine and 2-mercaptomethyl-3-guanidinoethylthiopropionic-acid

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 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 captopril did not affect arterial strips treated with Nomega-nitro-L-arginine. Angiotensin I-induced contractions was less reduced by captopril when the strips were pretreated with Nomega-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.

Topics: 3-Mercaptopropionic Acid; Angiotensin I; Angiotensin-Converting Enzyme Inhibitors; Animals; Bradykinin; Captopril; Dose-Response Relationship, Drug; Endothelium, Vascular; Enzyme Inhibitors; Iliac Artery; In Vitro Techniques; Nitric Oxide; Nitric Oxide Donors; Nitroarginine; Penicillamine; Peptidyl-Dipeptidase A; S-Nitroso-N-Acetylpenicillamine; Swine; Vasoconstriction; Vasodilation