Bianchini L, Fossat B, Porthé-Nibelle J, Ellory J C, Lahlou B
Laboratoire de Physiologie Cellulaire et Comparée et UA CNRS 651, Faculté des Sciences, Nice, France.
J Exp Biol. 1988 Jul;137:303-18. doi: 10.1242/jeb.137.1.303.
Isolated trout hepatocytes exposed to hypotonic Hank's medium (isotonicity x 0.70) swelled to 1.17 times the control volume after 3 min; by 15 min the cell volume had returned to normal. The ouabain-insensitive K+ uptake increased, indicating an immediate rise in K+ membrane permeability. As indicated by analysis of cellular contents, the regulatory volume decrease (RVD) was ensured by a release of intracellular K+. Na+ was not implicated in this mechanism. This potassium permeability induced by hypotonic shock was transient (maximum at 6 min), insensitive to blocking agents of voltage- and Ca2+-dependent K+ channels, and chloride-dependent. This result, together with a time-course of Cl- uptake similar to that of K+, suggests a K+/Cl- cotransport mechanism. This cotransport is inhibited by high furosemide concentrations (10(-3) mol l-1) but not by bumetanide (10(-4) mol l-1) or piretanide (10(-4) mol l-1).
将分离的鳟鱼肝细胞置于低渗的汉克氏培养基(等渗性为0.70)中,3分钟后细胞肿胀至对照体积的1.17倍;到15分钟时,细胞体积恢复正常。哇巴因不敏感的钾摄取增加,表明钾膜通透性立即升高。细胞内容物分析表明,调节性容积减小(RVD)是由细胞内钾的释放来确保的。钠不参与这一机制。低渗休克诱导的这种钾通透性是短暂的(6分钟时达到最大值),对电压依赖性和钙依赖性钾通道阻断剂不敏感,且依赖于氯。这一结果,连同与钾摄取相似的氯摄取时间进程,提示存在钾/氯共转运机制。这种共转运受到高浓度呋塞米(10⁻³ mol/L)的抑制,但不受布美他尼(10⁻⁴ mol/L)或吡咯他尼(10⁻⁴ mol/L)的抑制。