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Femtomolar bradykinin-induced relaxation of isolated bovine coronary arteries, mediated by endothelium-derived nitric oxide



Femtomolar bradykinin-induced relaxation of isolated bovine coronary arteries, mediated by endothelium-derived nitric oxide



Journal Of Veterinary Pharmacology & Therapeutics. 21(4): 304-308,.



We reported previously that bradykinin induces endothelium-dependent relaxation at nanomolar (nm) concentrations in isolated bovine coronary arteries with an intact endothelium. Recently we have found that in the presence of 10 muM indomethacin, femtomolar (fM) concentrations of bradykinin induce endothelium-dependent relaxation in some bovine coronary arteries (apprxeq 10% of the coronary arteries examined). The present study was designed to characterize the relaxation induced by fM bradykinin. Relaxation was completely abolished by repeated application of fM bradykinin, by 100 gm Nomega- nitro-L- arginine methyl ester and by 10 gm methylene blue. Relaxation induced by nM bradykinin was partly affected by these treatments. Relaxation induced by both concentrations of bradykinin was inhibited by a B2-kinin receptor antagonist, (Thi5,8, D-Phe 7)-bradykinin, in a concentration-dependent manner, but not by a B1-kinin receptor antagonist, des-Arg9, (Leu8)bradykinin. In the Relaxation was completely abolished by repeated application of fM bradykinin, by 100 muM Nomega- nitro-L- arginine methyl ester and by 10 muM methylene blue. Relaxation induced by nM bradykinin was partly affected by these treatments. Relaxation induced by both concentrations of bradykinin was inhibited by a B2-kinin receptor antagonist, (Thi5,8, D-Phe 7)-bradykinin, in a concentration-dependent manner, but not by a B1-kinin receptor antagonist, des-Arg9, (Leu8)bradykinin. In the presence of 10 muM captopril, an angiotensin-converting enzyme (ACE) inhibitor, all coronary arteries examined in this experiment showed endothelium-dependent relaxation to fM bradykinin. These results show that some bovine coronary arteries relax in response to fM bradykinin, and this response is mediated predominantly by the release of nitric oxide via stimulation of endothelial B2-kinin receptors. The relaxation may be dependent on ACE activity.

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Accession: 008682037

Download citation: RISBibTeXText

PMID: 9731953

DOI: 10.1046/j.1365-2885.1998.00141.x


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