Effect of membrane potential on furosemide-inhibitable sodium influxes in human red blood cells.
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.
Kracke
G R
GR
Department of Biology, Syracuse University, New York 13244.
Dunham
P B
PB
D000328:Adult; D004910:Erythrocyte Membrane / Q000187:drug effects / Q000502:physiology*; D005665:Furosemide / Q000494:pharmacology*; D006801:Humans; D008564:Membrane Potentials / Q000187:drug effects; D011188:Potassium / Q000097:blood; D012964:Sodium / Q000097:blood*; D013644:Tartrates / Q000494:pharmacology; D014634:Valinomycin / Q000494:pharmacology
D013644:Tartrates; D014634:Valinomycin; D005665:Furosemide; D012964:Sodium; D011188:Potassium