Miwa K, Schwartz A
Department of Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine, Ohio 45267.
Biochem Biophys Res Commun. 1987 Oct 14;148(1):1-8. doi: 10.1016/0006-291x(87)91068-0.
(-)Bay K 8644 produced a concentration-dependent contraction of porcine coronary artery rings with the maximal contraction at 10(-6) M. Pretreatment of the rings with 10(-6) M nitrendipine inhibited (-)Bay K 8644-induced contraction, while pretreatment with 10(-8) M nitrendipine potentiated the contraction elicited by (-)Bay K 8644. (-)Bay K 8644 (10(-6) M) significantly stimulated Ca2+ influx. Although 10(-8) M nitrendipine never stimulated Ca2+ influx, Ca2+ influx induced by (-)Bay K 8644 was significantly potentiated by pretreatment with 10(-8) M nitrendipine. Pretreatment with 10(-6) M nitrendipine significantly decreased Ca2+ influx in tissues treated with (-)Bay K 8644. Our results suggest that the increased Ca2+ influx might be involved in the mechanisms by which (-)Bay K 8644-induced contraction was potentiated by pretreatment with nitrendipine.
（-）Bay K 8644可使猪冠状动脉环产生浓度依赖性收缩，最大收缩出现在10^(-6) M时。用10^(-6) M尼群地平预处理冠状动脉环可抑制（-）Bay K 8644诱导的收缩，而用10^(-8) M尼群地平预处理则可增强（-）Bay K 8644引发的收缩。（-）Bay K 8644（10^(-6) M）可显著刺激Ca2+内流。虽然10^(-8) M尼群地平从未刺激Ca2+内流，但用10^(-8) M尼群地平预处理可显著增强（-）Bay K 8644诱导的Ca2+内流。用10^(-6) M尼群地平预处理可显著降低（-）Bay K 8644处理的组织中的Ca2+内流。我们的结果表明，Ca2+内流增加可能参与了尼群地平预处理增强（-）Bay K 8644诱导收缩的机制。
