Endothelium-dependent relaxation in perforating branch of human internal mammary artery.

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.