McLean A J, du Souich P, Barron K W, Briggs A H
J Pharmacol Exp Ther. 1978 Oct;207(1):40-8.
A study was made of the effects of hydralazine on K+ contractures in rabbit aortic strips. Measurements were made of effects on tension generation, Ca++ accumulation measured using 45Ca++ (lanthanum method) and 45Ca++ efflux. Hydralazine relaxed established K+ contractures and inhibited tension development when tissue exposure to hydralazine preceded K+ depolarization. Both the threshold and the maximum tension responses of strips to Ca++ (K+-depolarized tissues) were altered by hydralazine in a dose-dependent manner. The Ca++ uptake associated with K+ depolarization was inhibited by relaxant doses of hydralazine; however, hydralazine did not significantly affect the rate of 45Ca++ efflux. Hydralazine also raised the threshold to the inhibitory (relaxant) effects of higher (greater than 2.5 mM) bath concentrations of Ca++. It is suggested that hydralazine inhibits K+ contractures in aortic strips by interference with the entry of Ca++ into the cell, reflecting an effect of hydralazine at the cell surface membrane.
研究了肼屈嗪对兔主动脉条K⁺挛缩的影响。测量了其对张力产生的影响、使用⁴⁵Ca²⁺（镧法）测量的Ca²⁺蓄积以及⁴⁵Ca²⁺外流。当组织在K⁺去极化之前暴露于肼屈嗪时，肼屈嗪可使已形成的K⁺挛缩松弛并抑制张力发展。肼屈嗪以剂量依赖性方式改变了条带对Ca²⁺（K⁺去极化组织）的阈值和最大张力反应。与K⁺去极化相关的Ca²⁺摄取受到松弛剂量肼屈嗪的抑制；然而，肼屈嗪对⁴⁵Ca²⁺外流速率没有显著影响。肼屈嗪还提高了对较高（大于2.5 mM）浴液浓度Ca²⁺的抑制（松弛）作用的阈值。提示肼屈嗪通过干扰Ca²⁺进入细胞而抑制主动脉条的K⁺挛缩，这反映了肼屈嗪在细胞膜表面的作用。
