Karaki H
Department of Veterinary Pharmacology, Faculty of Agriculture, University of Tokyo, Japan.
Am J Hypertens. 1990 Aug;3(8 Pt 2):253S-256S. doi: 10.1093/ajh/3.8.253.
An increase in cytosolic Ca2+ level [( Ca2+]cyt) initiates smooth muscle contraction. Simultaneous measurements of [Ca2+]cyt and muscle tension provide insight into the Ca2+ regulation of smooth muscle. The photoprotein aequorin and the fluorescent Ca2+ indicator fura-2 have been used for this purpose. Although there are some differences between aequorin signal and fura-2 signal, comparison between [Ca2+]cyt and muscle tension in vascular smooth muscle indicates that high K+ and agonists that operate via specific receptors (receptor-agonists) induce sustained contraction whereas stimulated [Ca2+]cyt gradually decreases during prolonged exposure to agonists. Furthermore, greater contraction is produced by receptor-agonists than high K+ at a given [Ca2+]cyt. By contrast, cyclic AMP and cyclic GMP decrease muscle tension more strongly than [Ca2+]cyt. These results suggest that contractility of vascular smooth muscle is regulated not only by [Ca2+]cyt, but also by other mechanisms, possibly including Ca2+ sensitivity of the contractile elements. Ca2+ sensitization may be due to activation of protein kinase C.
胞质 Ca2+ 水平（[Ca2+]cyt）的升高引发平滑肌收缩。同时测量 [Ca2+]cyt 和肌肉张力有助于深入了解平滑肌的 Ca2+ 调节机制。为此已使用了光蛋白水母发光蛋白和荧光 Ca2+ 指示剂fura-2。尽管水母发光蛋白信号和fura-2信号存在一些差异，但对血管平滑肌中 [Ca2+]cyt 和肌肉张力的比较表明，高钾和通过特定受体起作用的激动剂（受体激动剂）会诱导持续收缩，而在长时间暴露于激动剂期间，受刺激的 [Ca2+]cyt 会逐渐降低。此外，在给定的 [Ca2+]cyt 水平下，受体激动剂比高钾产生更强的收缩。相比之下，环磷酸腺苷（cAMP）和环磷酸鸟苷（cGMP）降低肌肉张力的作用比降低 [Ca2+]cyt 的作用更强。这些结果表明，血管平滑肌的收缩性不仅受 [Ca2+]cyt 调节，还受其他机制调节，可能包括收缩元件对 Ca2+ 的敏感性。Ca2+ 致敏可能是由于蛋白激酶C的激活。
