Scharff O, Foder B
Department of Clinical Physiology and Nuclear Medicine, Rigshospitalet, Copenhagen, Denmark.
Eur J Pharmacol. 1989 Jan 10;159(2):165-73. doi: 10.1016/0014-2999(89)90701-2.
The effect of halothane on the Ca2+-sensitive K+ channel in human erythrocytes has been investigated. The red cells were suspended in buffer-free salt solutions containing Ca2+ or 45Ca2+. The protonophore CCCP was added to bring about a rapid equilibration of protons across the plasma membrane. After addition of the divalent cation ionophore A23187, the cells took up Ca2+ and this caused the K+ channels to open. When the medium contained 1 mM K+, the addition of A23187 induced a transient hyperpolarization of the cells, as monitored by measurement of the pH of the medium. The cellular pH, being buffered by haemoglobin, was virtually constant. Halothane reversibly inhibited hyperpolarization and limited the release of cellular K+ in a dose-dependent way, but did not inhibit the Ca2+-transporting properties of A23187. No stimulatory effects of halothane were observed even at low halothane concentrations. In conclusion, halothane reversibly inhibits the Ca2+-sensitive K+ channel in human erythrocytes with an ED50 of about 0.5 mM.
研究了氟烷对人红细胞中钙敏感性钾通道的影响。将红细胞悬浮于含有Ca2+或45Ca2+的无缓冲盐溶液中。加入质子载体CCCP以使质子快速跨质膜达到平衡。加入二价阳离子载体A23187后,细胞摄取Ca2+,这导致钾通道开放。当培养基中含有1 mM K+时,加入A23187会诱导细胞短暂超极化,通过测量培养基的pH值进行监测。由血红蛋白缓冲的细胞内pH值实际上是恒定的。氟烷可逆性抑制超极化,并以剂量依赖的方式限制细胞内钾的释放,但不抑制A23187的钙转运特性。即使在低氟烷浓度下也未观察到氟烷的刺激作用。总之,氟烷可逆性抑制人红细胞中的钙敏感性钾通道,半数有效浓度(ED50)约为0.5 mM。