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. 2000 Aug 1;116(2):299–310. doi: 10.1085/jgp.116.2.299

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© 2000 The Rockefeller University Press

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).

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Scheme illustrating the small-conductance K channel in the apical membrane of CCD was regulated by two different mechanisms: phosphorylation and dephosphorylation processes. Extracellular ATP stimulates G protein–coupled P₂Y₂ receptors, which potentiate the activity of PKG and increase the channel dephosphorylation through phosphatase (PP2A). Increasing channel phosphorylation processes can reverse the inhibitory effect of extracellular ATP on channel activity via activation of cAMP-dependent PKA.