Robertson B E, Schubert R, Hescheler J, Nelson M T
Department of Pharmacology, University of Vermont Medical Research Facility, Colchester 05446.
Am J Physiol. 1993 Jul;265(1 Pt 1):C299-303. doi: 10.1152/ajpcell.1993.265.1.C299.
Guanosine-3',5'-cyclic monophosphate (cGMP)-dependent protein kinase (cGMP-PK) plays a central role in the mediation of the vasodilator response to nitric oxide (NO) and other nitrovasodilators. It is unclear whether cGMP-PK affects calcium-activated potassium channels (KCa channels) or any other type of ion channel in smooth muscle. We provide here the first direct evidence that cGMP-PK can activate KCa channels in arterial smooth muscle cells. We demonstrate that NO and a membrane-permeable analogue of cGMP can activate KCa channels in on-cell patches approximately twofold. Furthermore, cGMP-PK, in the presence of ATP and cGMP added directly to the intracellular surface of inside-out patches, increases channel activity by approximately eightfold. These results suggest that cGMP-PK-mediated activation of KCa channels may contribute to the actions of NO and other nitrovasodilators.
3',5'-环磷酸鸟苷（cGMP）依赖性蛋白激酶（cGMP-PK）在介导血管舒张剂对一氧化氮（NO）和其他硝基血管舒张剂的反应中起核心作用。尚不清楚cGMP-PK是否影响钙激活钾通道（KCa通道）或平滑肌中的任何其他类型的离子通道。我们在此提供了第一个直接证据，证明cGMP-PK可以激活动脉平滑肌细胞中的KCa通道。我们证明，NO和cGMP的膜通透性类似物可以使膜片钳记录中的KCa通道活性增加约两倍。此外，在直接添加到外翻膜片胞内表面的ATP和cGMP存在下，cGMP-PK可使通道活性增加约八倍。这些结果表明，cGMP-PK介导的KCa通道激活可能有助于NO和其他硝基血管舒张剂的作用。
