Laher I, Vorkapic P, Dowd A L, Bevan J A
Department of Pharmacology, University of Vermont, Burlington 05405.
Biochem Biophys Res Commun. 1989 Nov 30;165(1):312-8. doi: 10.1016/0006-291x(89)91071-1.
The effects of PMA, an activator of protein kinase C, was studied on Ca2+-induced tone in the rabbit basilar artery. Contractile responses to Ca2+ occurred only in arteries pretreated with PMA; the extent of Ca2+-induced contractions were related to the level of stretch applied to the vessels. Bay K 8644, a Ca2+-channel agonist, at a concentration that was subthreshold for contraction, augmented the extent of Ca2+-induced tone occurring in PMA-treated arteries. Nifedipine, a Ca2+-entry inhibitor, and staurosporine, an inhibitor of protein kinase C attenuated the response to Ca2+ occurring either in the absence or presence of Bay K 8644. Our results suggest that PMA increases myofilament sensitivity to Ca2+, such that levels of Ca2+ previously ineffective for contraction Ca2+-influx, e.g. due to Bay K 8644, is manifest as contraction. Our results also confirm the role of extracellular Ca2+ entry via plasma membrane stretch-dependent Ca2+-channels in the maintenance of vascular tone in the basilar artery.
研究了蛋白激酶C激活剂佛波酯（PMA）对兔基底动脉中钙诱导张力的影响。对钙的收缩反应仅发生在用PMA预处理的动脉中；钙诱导收缩的程度与施加于血管的拉伸水平有关。钙通道激动剂Bay K 8644在低于收缩阈值的浓度下，增强了在PMA处理的动脉中发生的钙诱导张力的程度。钙内流抑制剂硝苯地平和蛋白激酶C抑制剂星形孢菌素减弱了在不存在或存在Bay K 8644时对钙的反应。我们的结果表明，PMA增加了肌丝对钙的敏感性，使得先前对收缩无效的钙水平（例如由于Bay K 8644导致的钙内流）表现为收缩。我们的结果还证实了通过质膜拉伸依赖性钙通道的细胞外钙内流在维持基底动脉血管张力中的作用。
