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Single-file diffusion through the Ca2+-activated K+ channel of human red cells
Authors:Bent Vestergaard-Bogind  Per Stampe  Palle Christophersen
Institution:(1) Department of Membrane Research, The Weizmann Institute of Science, 76100 Rehovot, Israel;(2) Present address: College of Arts and Sciences, University of Pennsylvania, 19104 Philadelphia, PA;(3) Present address: Departments of Physiology and Medicine, University of Pennsylvania School of Medicine, Richards Building/G4, 19104 Philadelphia, PA
Abstract:Summary We have examined the effect of internal and external pH on Na+ transport across toad bladder membrane vesicles. Vesicles prepared and assayed with a recently modified procedure (Garty & Asher, 1985) exhibit large, rheogenic, amiloridesensitive fluxes. Of the total22Na uptake measured 0.5–2.0 min after introducing tracer, 80±4% (mean±se,n=9) is blocked by the diuretic with aK 1 of 2×10–8 m. Thus, this amiloridesensitive flux is mediated by the apical sodium-selective channels. Varying the internal (cytosolic) pH over the physiologic range 7.0–8.0 had no effect on sodium transport; this result suggests that variation of intracellular pHin vivo has no direct apical effect on modulating sodium uptake. On the other hand,22Na was directly and monotonically dependent on external pH. External acidification also reduced the amiloride-sensitive efflux across the walls of the vesicles. This inhibition of22Na efflux was noted at external Na+ concentrations of both 0.2 mgrm and 53mm.These results are different from those reported with whole toad bladder. A number of possible bases for these differences are considered and discussed. We suggest that the natriferic response induced by mucosal acidification of whole toad urinary bladder appears to operate indirectly through one or more factors, presumably cytosolic, present in whole cells and absent from the vesicles.
Keywords:sodium channels  pH dependence  mucosal acidification  intracellular pH  apical Na+ entry  Na+ permeability
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