Effects of vasopressin and cAMP on single amiloride-blockable Na channels
- 1 May 1991
- journal article
- research article
- Published by American Physiological Society in American Journal of Physiology-Cell Physiology
- Vol. 260 (5), C1071-C1084
- https://doi.org/10.1152/ajpcell.1991.260.5.c1071
Abstract
To determine the mechanism by which vasopressin increases sodium transport in sodium-transporting, tight epithelia, we examined single amiloride-blockable Na channels in membrane patches from cultured distal nephron cells (A6) either before or after treatment with arginine vasopressin. Pretreatment of cells with vasopressin (40 mU/ml) for 40-50 min increases NPo (N, the number of Na channels; Po, the open probability of an individual Na channel). The increase in NPo is due to an increase in the number of conductive Na channels with little or no change in the open probability of individual Na channels. Pretreatment of cells for 1 h with 1 mM N6,2'-O-dibutyryladenosine 3', 5'-cyclic monophosphate (DBcAMP) also increased NPo. The increase in NPo caused by DBcAMP pretreatment is also due to the increase in the number of conductive Na channels with no change in the open probability of individual Na channels. Cells pretreated with cholera toxin (CTX; 250 ng/ml) for 4 h appeared similar to cells that had been treated with vasopressin or DBcAMP; that is, the number of Na channels per patch increased with little or no effect on the open probability of individual Na channels. For patches from many untreated cells, when the frequency of occurrence is plotted against the number of channels in an individual patch, the histogram consists of a single peak with a number of channels per patch of 2.0 +/- 1.5 (+/- SD, 126 patches). After pretreatment of cells with vasopressin, DBcAMP, or CTX, the same histogram contains two peaks after vasopressin of 1.8 +/- 1.2 and 9.2 +/- 1.5 (+/- SD, 38 and 53 patches, respectively). These observations suggest that pretreatment of cells with vasopressin, DBcAMP, or CTX may act by promoting insertion of clusters of new sodium channels.Keywords
This publication has 9 references indexed in Scilit:
- Effects of insulin and phosphatase on a Ca2(+)-dependent Cl- channel in a distal nephron cell line (A6).The Journal of general physiology, 1990
- [37] Cultures as epithelial models: Porous-bottom culture dishes for studying transport and differentiationMethods in Enzymology, 1989
- The role of membrane turnover in the water permeability response to antidiuretic hormoneThe Journal of Membrane Biology, 1988
- Mechanisms of aldosterone action in tight epitheliaThe Journal of Membrane Biology, 1986
- Amiloride-sensitive Na channels from the apical membrane of the rat cortical collecting tubule.Proceedings of the National Academy of Sciences, 1986
- Autoregulation of apical membrane Na+ permeability of tight epithelia. Noise analysis with amiloride and CGS 4270.The Journal of general physiology, 1985
- Hormonal control of apical membrane Na transport in epithelia. Studies with fluctuation analysis.The Journal of general physiology, 1983
- Amiloride-sensitive trypsinization of apical sodium channels. Analysis of hormonal regulation of sodium transport in toad bladder.The Journal of general physiology, 1983
- The role of sodium-channel density in the natriferic response of the toad urinary bladder to an antidiuretic hormoneThe Journal of Membrane Biology, 1982