Uski T K, Andersson K E
Acta Physiol Scand. 1985 Jan;123(1):49-53. doi: 10.1111/j.1748-1716.1985.tb07559.x.
The proposed calcium promotor BAY K 86(44) contracted feline basilar arteries partially depolarized by 10 mmol X 1(-1) potassium in a concentration-dependent manner (EC50 value: (2.1 +/- 1.2) X 10(-9) mol X 1(-1)). The concentration-response curve for prostaglandin (PG) F2 alpha was displaced to the left after pretreatment with BAY K 86(44). PGF2 alpha induced a biphasic contraction in calcium-free medium as has been described previously. The second PGF2 alpha-induced contraction phase in calcium-free medium was abolished by pretreatment with nifedipine or diltiazem. BAY K 86(44) restored the second phase in arteries pretreated with nifedipine, but not in vessels pretreated with diltiazem. The findings suggest that BAY K 86(44) acts as a promotor of calcium-influx, probably by interaction with the 'dihydropyridine receptor' in the cell membrane, and also provide support for the view that PGF2 alpha releases membrane-bound calcium.
所提出的钙促进剂BAY K 86(44) 以浓度依赖性方式使由10 mmol X 1(-1) 钾部分去极化的猫基底动脉收缩（半数有效浓度值：(2.1 +/- 1.2) X 10(-9) mol X 1(-1)）。用BAY K 86(44) 预处理后，前列腺素（PG）F2α 的浓度-反应曲线向左移位。如先前所述，PGF2α 在无钙培养基中诱导双相收缩。无钙培养基中PGF2α 诱导的第二个收缩相被硝苯地平或地尔硫䓬预处理所消除。BAY K 86(44) 恢复了用硝苯地平预处理的动脉中的第二个收缩相，但在用地尔硫䓬预处理的血管中未恢复。这些发现表明BAY K 86(44) 作为钙内流的促进剂，可能是通过与细胞膜中的“二氢吡啶受体”相互作用，并且也支持了PGF2α 释放膜结合钙的观点。
