We examined mechanisms of relaxation in intact and endothelium-denuded thoracic aortic rings of rat in response to various concentrations of calcium (from 1.6 to 10.1 mM) after contraction induced by 30 mM KCl. The relaxation to calcium was concentration dependent in intact and denuded rings. This effect was greater in intact preparations than in denuded preparations or in intact preparations treated with methylene blue (10(-5) M). This indicates that the relaxation by calcium is partly mediated by releasing endothelium-derived relaxing factors (EDRFs). In the presence of A23187, the relaxation to calcium was attenuated in intact rings but not in denuded rings, whereas calcium relaxation was not significantly altered by sodium nitroprusside. These observations suggest that the calcium-induced relaxation is reduced if EDRF has already been released by A23187. We conclude that, paradoxically, the same increase in extracellular Ca2+ concentration that causes an increase in endothelial intracellular calcium concentration ([Ca2+]i) to produce EDRF also results in membrane stabilization of the vascular smooth muscle cell to decrease [Ca2+]i and cause relaxation. These two mechanisms are additive in producing calcium relaxation in the intact artery.
- Copyright © 1991 the American Physiological Society