Heaslip R J, Rahwan R G
Can J Physiol Pharmacol. 1982 May;60(5):743-6. doi: 10.1139/y82-103.
The aim of the present investigation was to elucidate the pharmacological mechanism by which U44069, a stable PGH2 analogue, contracts the rat aorta. The results obtained demonstrate that while the contractile effect of potassium chloride is obliterated by removal of extracellular calcium, a substantial proportion of the contractile effect of U44069 persists under these conditions. The persistent effect of U44069 under calcium-free conditions was not diminished by nifedipine (a slow calcium channel blocker) but was blocked by 2-n-butyl-3-dimethylamino-5,6-methylenedioxyindene (an intracellular calcium antagonist). These results provide experimental evidence for the proposal that U44069 contracts the aorta in the absence of extracellular calcium by mobilizing intracellular calcium.
本研究的目的是阐明稳定的前列环素H2（PGH2）类似物U44069使大鼠主动脉收缩的药理机制。所获得的结果表明，虽然通过去除细胞外钙可消除氯化钾的收缩作用，但在这些条件下，U44069的收缩作用仍有很大一部分持续存在。在无钙条件下U44069的持续作用不受硝苯地平（一种慢钙通道阻滞剂）的影响，但被2-正丁基-3-二甲氨基-5,6-亚甲基二氧茚（一种细胞内钙拮抗剂）阻断。这些结果为以下提议提供了实验证据，即U44069通过动员细胞内钙在无细胞外钙的情况下使主动脉收缩。
