Van Wagoner D R, Kirian M, Lamorgese M
Department of Molecular Cardiology, Cleveland Clinic Foundation, Ohio 44195-5069, USA.
Am J Physiol. 1996 Sep;271(3 Pt 2):H937-46. doi: 10.1152/ajpheart.1996.271.3.H937.
The modulation of whole cell K+ currents by the alpha 1-adrenergic agonist, phenylephrine, was studied in isolated rat atrial myocytes by use of perforated-patch whole cell recording techniques. The out ward K+ current in these myocytes consists of two inactivating components (iK,f and iK,s), which differ in the kinetics of inactivation and recovery from inactivation, and a noninactivating component, (iK,ss). Superfusion of these myocytes with 10 microM phenylephrine caused a rapid suppression of iK,ss, with little effect on the other current components. This effect of phenylephrine could be mimicked by exogenous application of 1,2-dioctanoyl-sn-glycerol (20 microM), a membrane-permeant diacylglycerol analogue; however, it was clearly distinct from the effect of 5 nM alpha-dendrotoxin, which selectively suppressed the slowly inactivating current component, iK,s, while having no effect on iK,ss. At a dose of 50 microM, phenylephrine also suppressed iK,s. There was no significant effect of phenylephrine (10 or 50 microM) or alpha-dendrotoxin (5 nM) on the rapidly inactivating current component, iK,f. The kinetic and pharmacological differences between these current components suggest that they represent the activity of distinct K+ channels.
运用穿孔膜片全细胞记录技术，在分离的大鼠心房肌细胞中研究了α1 - 肾上腺素能激动剂去氧肾上腺素对全细胞钾电流的调节作用。这些心肌细胞中的外向钾电流由两个失活成分（快速失活钾电流iK,f和缓慢失活钾电流iK,s，二者在失活动力学及从失活状态恢复的过程方面存在差异）以及一个非失活成分（持续钾电流iK,ss）组成。用10微摩尔/升的去氧肾上腺素灌注这些心肌细胞，可迅速抑制iK,ss，而对其他电流成分影响甚微。去氧肾上腺素的这种作用可被外源性施加的1,2 - 二辛酰 - sn - 甘油（20微摩尔/升，一种可透过细胞膜的二酰甘油类似物）模拟；然而，它与5纳摩尔α - 银环蛇毒素的作用明显不同，后者选择性抑制缓慢失活电流成分iK,s，而对iK,ss无影响。在50微摩尔/升的剂量下，去氧肾上腺素也抑制iK,s。去氧肾上腺素（10或50微摩尔/升）或α - 银环蛇毒素（5纳摩尔）对快速失活电流成分iK,f均无显著影响。这些电流成分在动力学和药理学上的差异表明它们代表了不同钾通道的活性。
