Karaki H, Ahn H Y, Urakawa N
Arch Int Pharmacodyn Ther. 1987 Jan;285(1):60-71.
Characteristics of caffeine-induced contraction were compared with those of high K+- and norepinephrine-induced contractions in order to evaluate the participation of the Ca++-induced Ca++-release (CCR) from storage site in the vascular smooth muscle of rabbit aorta. Caffeine induced a transient contraction in a solution without MgCl2. One mM Mg++ selectively inhibited the caffeine-induced contraction. Two mM procaine inhibited the contractions induced by caffeine, high K+ and norepinephrine. One mM lidocaine and low temperature (23 degrees C) inhibited both high K+- and norepinephrine-induced contractions but rather potentiated the caffeine-induced contraction. Simultaneous addition of 10(-6) M verapamil and 10(-5) M sodium nitroprusside inhibited both high K+- and norepinephrine-induced contractions, but not the caffeine-induced contraction. In a Ca++-free solution, both caffeine and norepinephrine induced transient contractions. Norepinephrine-induced transient contraction was more strongly inhibited than caffeine-induced contraction by 2 mM procaine and 1 mM lidocaine, whereas 5 mM Mg++ inhibited only the caffeine-induced contraction. In sarcoplasmic reticulum of skeletal muscle, it has been shown that the CCR is activated by caffeine and inhibited by procaine, but not by lidocaine and low temperature. Although Mg++ is an inhibitor of CCR, changes in extracellular Mg++ concentrations do not seem to readily modify the intracellular Mg++ concentration in the intact smooth muscle, and the inhibitory effect of Mg++ on caffeine-induced contraction may not be attributable to the direct effect on sarcoplasmic reticulum. These results suggest that the CCR plays an important role in the contraction induced by caffeine but not in the contractions induced by high K+ and norepinephrine in the vascular smooth muscle of rabbit aorta.
为了评估储存部位的钙离子诱导的钙离子释放（CCR）在兔主动脉血管平滑肌收缩中的参与情况，将咖啡因诱导的收缩特性与高钾和去甲肾上腺素诱导的收缩特性进行了比较。在不含氯化镁的溶液中，咖啡因诱导了短暂的收缩。1 mM镁离子选择性地抑制了咖啡因诱导的收缩。2 mM普鲁卡因抑制了咖啡因、高钾和去甲肾上腺素诱导的收缩。1 mM利多卡因和低温（23摄氏度）抑制了高钾和去甲肾上腺素诱导的收缩，但却增强了咖啡因诱导的收缩。同时添加10(-6) M维拉帕米和10(-5) M硝普钠抑制了高钾和去甲肾上腺素诱导的收缩，但不抑制咖啡因诱导的收缩。在无钙溶液中，咖啡因和去甲肾上腺素都诱导了短暂的收缩。2 mM普鲁卡因和1 mM利多卡因对去甲肾上腺素诱导的短暂收缩的抑制作用比对咖啡因诱导的收缩更强，而5 mM镁离子仅抑制咖啡因诱导的收缩。在骨骼肌的肌浆网中，已表明CCR被咖啡因激活并被普鲁卡因抑制，但不受利多卡因和低温抑制。尽管镁离子是CCR的抑制剂，但细胞外镁离子浓度的变化似乎不容易改变完整平滑肌细胞内的镁离子浓度，镁离子对咖啡因诱导收缩的抑制作用可能并非归因于对肌浆网的直接作用。这些结果表明，CCR在兔主动脉血管平滑肌中咖啡因诱导的收缩中起重要作用，但在高钾和去甲肾上腺素诱导的收缩中不起作用。
