Department of Neurology, College of Medicine, Chosun University, Gwangju 501-759, Korea.
Korean J Physiol Pharmacol. 2008 Feb;12(1):25-30. doi: 10.4196/kjpp.2008.12.1.25. Epub 2008 Feb 28.
Although many studies show that thromboxane A(2) (TXA(2)) has the action of gastrointestinal (GI) motility using GI muscle cells and tissue, there are no reports on the effects of TXA(2) on interstitial cells of Cajal (ICC) that function as pacemaker cells in GI tract. So, we studied the modulation of pacemaker activities by TXA(2) in ICC with whole cell patch-clamp technique. Externally applied TXA(2) (5microM) produced membrane depolarization in current-clamp mode and increased tonic inward pacemaker currents in voltage-clamp mode. The tonic inward currents by TXA(2) were inhibited by intracellular application of GDP-beta-S. The pretreatment of ICC with Ca(2+) free solution and thapsigargin, a Ca(2+)-ATPase inhibitor in endoplasmic reticulum, abolished the generation of pacemaker currents and suppressed the TXA(2)-induced tonic inward currents. However, chelerythrine or calphostin C, protein kinase C inhibitors, did not block the TXA(2)-induced effects on pacemaker currents. These results suggest that TXA(2) can regulate intestinal motility through the modulation of ICC pacemaker activities. This modulation of pacemaker activities by TXA(2) may occur by the activation of G protein and PKC independent pathway via extra and intracellular Ca(2+) modulation.
尽管许多研究表明血栓素 A2(TXA2)通过胃肠道(GI)肌肉细胞和组织具有胃肠道动力作用,但尚无关于 TXA2 对作为胃肠道起搏细胞的 Cajal 间质细胞(ICC)的影响的报道。因此,我们使用全细胞膜片钳技术研究了 TXA2 对 ICC 起搏活动的调节作用。在电流钳模式下,外源性 TXA2(5μM)可引起细胞膜去极化,并在电压钳模式下增加紧张性内向起搏电流。TXA2 引起的紧张性内向电流可被细胞内 GDP-β-S 抑制。用无钙溶液和内质网中 Ca2+-ATP 酶抑制剂 thapsigargin 预处理 ICC,可消除起搏电流的产生,并抑制 TXA2 诱导的紧张性内向电流。然而,蛋白激酶 C 抑制剂 chelerythrine 或 calphostin C 并不能阻断 TXA2 对起搏电流的影响。这些结果表明,TXA2 可通过调节 ICC 起搏活动来调节肠道动力。TXA2 对起搏活动的这种调节可能通过细胞外和细胞内 Ca2+调节,通过激活 G 蛋白和 PKC 非依赖性途径来发生。