Morimoto S, Koh E, Kim S, Morita R, Fukuo K, Ogihara T
Department of Medicine and Geriatrics, Osaka University Medical School, Japan.
Am J Hypertens. 1990 Aug;3(8 Pt 2):241S-244S. doi: 10.1093/ajh/3.8.241.
The possible mechanism of action of prostaglandin F2 alpha on vascular smooth muscle was investigated. Prostaglandin F2 alpha induced sustained tonic vasoconstriction of rat aortic strips, accompanied by rapid increase in the cytosolic free Ca2+ concentration [( Ca2+]i) in the vascular smooth muscle cells. Prostaglandin F2 alpha also evoked rapid increase in production of inositol 1,4,5,-trisphosphate (Ins-P3). Moreover, it increased release of Ca2+ from nonmitochondrial pools in digitonin-permeabilized vascular smooth muscle cells, although this effect was much weaker than that of Ins-P3. These results suggest that the sustained action of prostaglandin F2 alpha may involve not only a rise in [Ca2+]i mediated by Ins-P3, but also a direct stimulation of Ca2+ from intracellular stores.
研究了前列腺素F2α对血管平滑肌的可能作用机制。前列腺素F2α可引起大鼠主动脉条的持续性强直血管收缩，同时血管平滑肌细胞胞质游离Ca2+浓度[Ca2+]i迅速升高。前列腺素F2α还能引起肌醇1,4,5-三磷酸（Ins-P3）生成的快速增加。此外，它能增加洋地黄皂苷通透的血管平滑肌细胞中非线粒体钙池的Ca2+释放，尽管这种作用比Ins-P3的作用弱得多。这些结果表明，前列腺素F2α的持续作用可能不仅涉及由Ins-P3介导的[Ca2+]i升高，还涉及对细胞内钙库Ca2+的直接刺激。
