Imai S, Nakazawa M, Imai H, Nabata H
Arch Int Pharmacodyn Ther. 1984 Sep;271(1):98-105.
In order to search into the mechanism of the potassium contracture of the dog coronary artery the effects of procaine were studied in the isolated smooth muscle preparation of the dog coronary artery. Procaine is a substance which is known to specifically inhibit the calcium-induced calcium release mechanism. A dose-related relaxation of the potassium contracture was observed with procaine. However, the increase in La3+-resistant 45Ca uptake as measured by the Karaki and Weiss' method (1979) was not inhibited. As reported in a previous paper, caffeine induced a phasic contraction of the fully-depolarized preparation in a calcium-free EGTA containing medium. Procaine produced a dose-related inhibition of this contraction. These findings suggest that the potassium contracture of the dog coronary artery is dependent on the calcium-induced calcium release mechanism. Since the potassium contracture of this preparation can be relaxed by calcium antagonists, it may be inferred that the calcium influx through the voltage-dependent channels may represent the initiation mechanism of the calcium-induced calcium release process.
为了探究犬冠状动脉钾挛缩的机制,我们在犬冠状动脉离体平滑肌标本中研究了普鲁卡因的作用。已知普鲁卡因是一种能特异性抑制钙诱导钙释放机制的物质。观察到普鲁卡因可使钾挛缩呈剂量依赖性舒张。然而,用Karaki和Weiss(1979年)的方法测定的镧抗性45钙摄取增加并未受到抑制。如前一篇论文所报道,咖啡因在无钙EGTA培养基中诱导完全去极化标本出现阶段性收缩。普鲁卡因对这种收缩产生剂量依赖性抑制。这些发现表明犬冠状动脉的钾挛缩依赖于钙诱导钙释放机制。由于该标本的钾挛缩可被钙拮抗剂舒张,因此可以推断通过电压依赖性通道的钙内流可能代表钙诱导钙释放过程的起始机制。