Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
PLoS One. 2013 May 14;8(5):e63337. doi: 10.1371/journal.pone.0063337. Print 2013.
Cardiac KATP channels link metabolism with electrical activity. They are implicated in arrhythmias, secretion of atrial natriuretic peptide and protection of the heart from hypertrophy and failure. These processes may involve mechanosensitivity. KATP channels can be activated by mechanical stimulation and disrupting the cortical actin increases the activity. We propose that KATP channels are modulated by local bilayer tension and this tension is affected by cortical F-actin. Here we measured KATP background activity and stretch sensitivity with inside-out patches of rat ventricular myocytes before and after disrupting F-actin. Disrupting F-actin potentiated background activity but did not influence the slope sensitivity in the semilog relationship of NPo vs. suction that is a measure of the change in dimensions between closed and open states. Thus actin alters prestress on the channel probably by parallel elastic sharing of mean cortical tension with the bilayer.
心脏 KATP 通道将代谢与电活动联系起来。它们与心律失常、心房利钠肽的分泌以及心脏肥大和衰竭的保护有关。这些过程可能涉及机械敏感性。KATP 通道可被机械刺激激活，破坏皮质肌动蛋白会增加其活性。我们提出，KATP 通道受到局部双层张力的调节，而这种张力受皮质 F-肌动蛋白的影响。在这里，我们在破坏 F-肌动蛋白前后测量了大鼠心室肌细胞的内外向片上的 KATP 背景活性和拉伸敏感性。破坏 F-肌动蛋白增强了背景活性，但对半对数关系 NPo 与抽吸的斜率敏感性没有影响，这是衡量关闭和开放状态之间尺寸变化的指标。因此，肌动蛋白可能通过与双层膜平均皮质张力的并联弹性共享来改变通道的预张力。
