Calcium Channel Activation Does Not Increase Release of Endothelial-Derived Relaxant Factors (EDRF) in Rat Aorta Although Tonic Release of EDRF May Modulate Calcium Channel Activity in Smooth Muscle

Abstract

We investigated whether Ca2+ channel activation by K+ or Bay K 8644 could cause release of endothelium-derived relaxant factor (EDRF) from rat aorta. Bay K 8644 (0.1–100 nM) did not relax rat aorta preparations partially contracted with phenylephrine, although acetylcholine caused large relaxations. Following partial K +-depolarization (12 or 15 m M), Bay K 8644 (10 n M-1 μ M) contracted rat aorta preparations directly. Preparations were more sensitive to Bay K 8644 when stripped of the endothelium in 12 m M K+; concentration-effect curves were displaced to the left, and maximum responses were enhanced. In 15 m M K +, there was a leftward shift of the curves without change of maximal responses. However, Bay K 8644 (1 μ M), did not increase the guanosine 3‘,5’ cyclic-monophosphate (cGMP) content of rat aorta in the presence of endothelium, which is a function of EDRF release.