Morimoto S, Kim S, Fukuo K, Koh E, Morita R, Kitano S, Miyashita Y, Imanaka S, Ogihara T
Department of Geriatric Medicine, Osaka University Medical School, Japan.
Eur J Pharmacol. 1990 Jun 12;188(6):369-78. doi: 10.1016/0922-4106(90)90197-6.
The roles of intracellular free Ca2+ and protein kinase C in the tonic contraction induced by prostaglandin were studied. Prostaglandin F2 alpha induced tonic contraction of rat thoracic aorta in both control and Ca2(+)-free solution. Close correlations were observed between the contractile response of aortic strips and the changes in intracellular free Ca2+ concentration in vascular smooth muscle cells assessed with the fluorescent Ca2+ indicator fura 2, both in control and Ca2(+)-free solutions. Prostaglandin F2 alpha also enhanced the production of inositol 1,4,5-trisphosphate in vascular smooth muscle cells before the rise of the intracellular free Ca2+ concentration. Moreover, 1-(5-isoquinoline-sulfonyl)-2-methylpiperazine, an inhibitor of protein kinase C, inhibited the tonic contractions induced by PGF2 alpha and 12-O-tetradecanoyl phorbol-13-acetate, a direct activator of protein kinase C, at similar concentrations. These results suggest that both intracellular free Ca2+ and protein kinase C participate in prostaglandin F2 alpha-induced tonic contraction.
研究了细胞内游离钙离子（Ca2+）和蛋白激酶C在前列腺素诱导的强直性收缩中的作用。在对照溶液和无Ca2+溶液中，前列腺素F2α均可诱导大鼠胸主动脉的强直性收缩。在用荧光Ca2+指示剂fura 2评估的情况下，无论是在对照溶液还是无Ca2+溶液中，均观察到主动脉条的收缩反应与血管平滑肌细胞内游离Ca2+浓度变化之间存在密切相关性。在细胞内游离Ca2+浓度升高之前，前列腺素F2α还增强了血管平滑肌细胞中肌醇1,4,5-三磷酸的生成。此外，蛋白激酶C抑制剂1-（5-异喹啉磺酰基）-2-甲基哌嗪在相似浓度下可抑制前列腺素F2α和蛋白激酶C的直接激活剂12-O-十四烷酰佛波醇-13-乙酸酯诱导的强直性收缩。这些结果表明，细胞内游离Ca2+和蛋白激酶C均参与了前列腺素F2α诱导的强直性收缩。
