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Effects of endothelium‐derived constricting factor and calcium antagonists on calcium uptake into aortic vascular smooth muscle cells

Edothelial cells in culture secrete a protein termed endothelium‐derived constricting factor (EDCF) that elicits vasoconstriction in isolated arteries. In this study, the effect of EDCF on Ca2+ influx into cultured rat aortic smooth muscle cells and on force development in coronary arteries was evaluated and compared to that elicited by depolarization with K+. In addition, the effects of the Ca2+ antagonists bepridil, verapamil, and nitrendipine on EDCF‐ and K+‐induced changes in smooth muscle Ca2+ uptake and contractile force were also quantified and compared. EDCF, but not conditioned media from control cultures of fibroblasts or pituitary cells, enhanced Ca2+ influx into monolayer cultures of rat aortic smooth muscle cells in a time‐ and dose‐dependent manner. The time course of Ca2+ uptake in response to EDCF was similar to that elicited by K+. EDCF also resulted in a time‐ and dose‐dependent increase in isometric force in isolated deendothelialized rings of porcine coronary artery, which was more resistant to washout than that induced by K+. The increase in both Ca2+ influx and isometric tension induced by EDCF was abolished by heating the EDCF preparation to 80°C for 15 min. Bepridil (10 m̈M), verapamil (1 m̈M), and nitrendipine (1 m̈M) either markedly attenuated or completely blocked both EDCF‐ and K+‐induced increases in Ca2+ uptake and contractile force. The similarity between the effect of the Ca2+ antagonists on K+‐ and EDCF‐induced changes in vascular smooth muscle function suggests that a site of action of EDCF may be directed at the voltage‐sensitives Ca2+ channel.