Endothelium-dependent relaxation in perforating branch of human internal mammary artery |
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Authors: | Pesić S Jovanović A Grbović L Inić M Munjas N |
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Affiliation: | Department of Pharmacology, Medical Faculty, Bra?e Taskovi? 81, 18000, Nis-YU, Yugoslavia. |
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Abstract: | The purpose of the present study was to examine the effect of acetylcholine on perforating branch of the human internal mammary artery (HIMA). Acetylcholine (10(-9)-10(-5)M) induced concentration- and endothelium-dependent relaxation (pEC(50)=7.54+/-0.03, maximal response was 98+/-1.3%) of the precontracted arterial segments. Indomethacin, 4-aminopyridine (10(-5)M) and precontraction with K(+)-rich Krebs-Ringer-bicarbonate solution had no effect on acethylcholine-induced relaxation. N(G)-monomethyl-L-arginine (L-NMMA) (10(-5)M) inhibited relaxation evoked by acetylcholine. Indomethacin applied together with L-NMMA lead to further inhibition of acethylcholine-induced relaxation. Even in the presence of both L-NMMA and indomethacin, 4-aminopyridine had no provoked further inhibition of acetylcholine-induced relaxation of perforating branch of HIMA. It was concluded that the acethylcholine-induced relaxation of isolated perforating branch of HIMA is probably mediated via endothelial production of nitric oxide. However, when NO-synthase is inhibited, acetylcholine-induced vasorelaxation may be, in part, mediated through activation of cyclooxygenase pathway and consequent production and release of prostacyclin or some other cyclooxygenase products. |
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