Iino M, Kobayashi T, Endo M
Department of Pharmacology, Faculty of Medicine, University of Tokyo, Japan.
Biochem Biophys Res Commun. 1988 Apr 15;152(1):417-22. doi: 10.1016/s0006-291x(88)80730-7.
Calcium store of the skinned fibers of the guinea-pig portal vein, pulmonary artery and taenia caeci consisted of two classes: one with both Ca-induced Ca release (CICR) and inositol 1,4,5-trisphosphate (IP3)-induced Ca release (IICR) mechanisms (S alpha) and the other only with IICR mechanisms (S beta). Ryanodine, applied during the CICR was activated, locked the CICR channels open, but the drug had practically no effect on the IICR mechanism. Thus, after the ryanodine treatment the Ca store with the CICR (S alpha) lost its capacity to hold Ca. Changes in the agonist-evoked contraction of intact muscle due to the ryanodine treatment suggest that agonists release Ca from S alpha which produces the initial phase of contractures.
豚鼠门静脉、肺动脉和盲肠带皮纤维的钙储存由两类组成:一类同时具有钙诱导钙释放(CICR)和肌醇1,4,5-三磷酸(IP3)诱导钙释放(IICR)机制(Sα),另一类仅具有IICR机制(Sβ)。在CICR被激活期间应用的ryanodine可锁定CICR通道使其开放,但该药物对IICR机制几乎没有影响。因此,在ryanodine处理后,具有CICR的钙储存(Sα)失去了储存钙的能力。ryanodine处理导致的完整肌肉激动剂诱发收缩的变化表明,激动剂从Sα释放钙,从而产生挛缩的初始阶段。