McLean A J, Barron K, du Souich P, Haegele K D, McNay J L, Carrier O, Briggs A
J Pharmacol Exp Ther. 1978 May;205(2):418-25.
The mechanism of action and relative potency of hydralazine (H) and tow hydrazone derivatives were investigated using isolated rabbit aortic strips. H, hydralazine acetone hydrazone (HA) and hydralazine butanone hydrazone (HBH) relaxed established K+ and norepinephrine (NE) contractures, and inhibited the development of contractures to these two agents on preincubation. H, HA and HBH increased the threshold to Ca++ and decreased the maximum tension responses during K+-Ca++-contractures (HA greater than H, P less than .05; HBH greater than H P less than .01). The Ca++-dependent and Ca++-independent components of NE contractures were both inhibited by H, HA and HBH. NE contractures were more sensitive to the effects of H than K+ contractures. These results are consistent with the conclusion that H and hydrazone derivatives produce effects on vascular muscle both by interactions with the fluxes of Ca++ from the extracellular space and effects on release from cell stores. However, other possibilities need to be assessed experimentally.
使用离体兔主动脉条研究了肼屈嗪（H）及两种腙衍生物的作用机制和相对效价。H、丙酮腙肼屈嗪（HA）和丁酮腙肼屈嗪（HBH）可使已形成的钾离子（K⁺）和去甲肾上腺素（NE）收缩反应舒张，并在预孵育时抑制对这两种药物的收缩反应的发展。H、HA和HBH提高了钙离子（Ca²⁺）阈值，并降低了K⁺-Ca²⁺收缩过程中的最大张力反应（HA大于H，P小于0.05；HBH大于H，P小于0.01）。H、HA和HBH均抑制了NE收缩反应中依赖Ca²⁺和不依赖Ca²⁺的成分。NE收缩反应比K⁺收缩反应对H的作用更敏感。这些结果与以下结论一致：H和腙衍生物通过与细胞外空间Ca²⁺通量相互作用以及对细胞内储存释放的影响，对血管平滑肌产生作用。然而，其他可能性需要通过实验进行评估。
