Different involvement of endothelium-derived relaxing factor and prostacyclin in vasodilator response to bradykinin in isolated dog blood vessels.

Abstract

The study presented so far demonstrates that there is a heterogeneity in the mechanisms of vasodilator action of BK in various dog blood vessels (coronary vs mesenteric artery, and mesenteric artery vs vein). The different mechanisms underlying the BK-induced vasodilatation are summarized in Fig. 3. Three mechanisms are at least involved; 1) EDRF-release from endothelial cells which may not be mediated by B1 receptor, but presumably by B2 receptor, 2) PGI2-release from endothelial cells, 3) PGI2-release from smooth muscle (subendothelial) cells. The PGI2-release may be mediated by B1 receptor. Vasodilatation caused by BK is mediated via "1" in coronary arteries, "2" + "3" in mesenteric veins, and "1" + "2" + "3" in mesenteric and renal arteries in the dog. Another reasons for the differences in the BK-induced vasodilatation may be different number or sensitivity of BK receptors located on the endothelial and smooth muscle cells, or the responsiveness of the vascular smooth muscle cells to the intermediate vasodilator substances and BK itself.