Kracke G R, Dunham P B
Department of Biology, Syracuse University, New York 13244.
J Membr Biol. 1987;98(2):117-24. doi: 10.1007/BF01872124.
Furosemide-inhibitable Na influx (a measure of Na/K/Cl cotransport) was determined as a function of membrane potential in human red blood cells. The membrane potential was varied from -42 to +118 mV using valinomycin and gradients of K. The furosemide-inhibitable, unidirectional Na influx was independent of membrane potential over the entire range of potentials. The change in flux per mV, 0.443 mumol/(liter cells.hr.mV), was not significantly different from zero. The mean flux was 153 +/- 16 mumol/(liter cells.hr) (+/- SEM, n = 71). The ouabain and furosemide-resistant influxes of Na and K were also measured as functions of membrane potential using either valinomycin and K or a chloride-free, tartrate flux medium to vary membrane potential. The unidirectional Na influx decreased slightly as the membrane potential was increased from negative potentials to about +10 mV. At higher membrane potentials Na influx rose dramatically with potential. This increase was not reversible and was also observed with K influx.
在人红细胞中，测定了速尿可抑制的钠内流（钠/钾/氯共转运的一种测量指标）作为膜电位的函数。使用缬氨霉素和钾梯度将膜电位从-42mV改变至+118mV。在整个电位范围内，速尿可抑制的单向钠内流与膜电位无关。每毫伏通量的变化为0.443微摩尔/（升细胞·小时·毫伏），与零无显著差异。平均通量为153±16微摩尔/（升细胞·小时）（±标准误，n = 71）。还使用缬氨霉素和钾或无氯、酒石酸盐通量介质来改变膜电位，并测定了哇巴因和速尿抗性的钠和钾内流作为膜电位的函数。随着膜电位从负电位增加到约+10mV，单向钠内流略有下降。在更高的膜电位下，钠内流随电位急剧上升。这种增加是不可逆的，钾内流也观察到了这种情况。
