MECHANISMS OF THE VASCULAR WALL CALCIUM RELAXATION

Using the method of the measuring the isometric tension of isolated bl ood vessels we investigated some mechanisms of action of high calcium concentration (>3 mM) on the mechanical activity of small branches of the rat mesenteric artery. Calcium in concentrations up to 30 mM cause d the relaxation of the arteries (calcium relaxation). The effect ampl itude decreased in the presence of ouabain (10(-4) M), tetraethylammon ium (10(-3) M), charibdotoxin (10(-7) M) and in the potassium-free ext ernal solution in intact and denuded rings. Glibenclamide (10(-6) M), 4-aminopyridine (10(-3) M), barium (10(-3) M) and cesium (2 . 10(-2) M ) were inefficient. Calcium relaxation of intact vessels was impaired in the presence of N-omega-nitro-L-arginine (10(-4) M) or methylene bl ue (10(-4) M), but not in the presence of indomethacin (10(-5) M). The attenuation to the same extent of calcium relaxation was observed in denuded mesenteric arteries. We conclude that calcium can causes the r elaxation of the vascular smooth muscle cells by two mechanisms. The f irst one is mediated via the cell membrane hyperpolarization due to th e activation of Na+/K+-ATP-ase and Ca2+-activated potassium channels. The second mechanism is endothelium-mediated and depends on the nitric oxide - guanilate cyclase pathway.