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Amiloride inhibits the vasopressin-induced increase in epithelial water permeability

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Abstract

The vasopressin (VP)-induced increase in water permeability in high-resistance, amphibian epithelia is not altered by the abolition of net Na+ flux caused by amiloride added to the apical bathing medium. In this work we looked at the effects on water transport of amiloride added to the serosal medium at a concentration (10−3 M) known to inhibit Na+/H + exchange. In urinary bladders of Bufo marinus, amiloride partially blocked the hydrosmotic response to VP. A similar inhibition was found with cyclic adenosine 5′-monophosphate (cAMP) or serosal hypertonicity. We hypothesized that this effect of amiloride could be due to an inhibition of Na+/H+ and/or Na+/Ca2+ antiporters present in the epithelial basolateral membrane and looked at the effects of the diuretic in Na+-free media. A similar degree of inhibition of water flow was still found, thus showing that amiloride acts on a cell target other than the antiporters. In toad skin, amiloride did not inhibit the hydrosmotic response to VP and to isoproterenol; however the response to high K+ was significantly reduced. Among the amiloride cell targets described so far, adenylate cyclase and protein kinase A appear to be the best candidates to explain the inhibition of the hydrosmotic response reported here. Direct measurements of intracellular cAMP are needed however to substantiate this hypothesis.

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Grosso, A., Cragoe, E.J. & DeSousa, R.C. Amiloride inhibits the vasopressin-induced increase in epithelial water permeability. Pflugers Arch. 417, 200–206 (1990). https://doi.org/10.1007/BF00370700

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