Possible Involvement of Phosphorylation/Dephosphorylation in the Regulation of Epithelial Sodium Channels
Luminal Na+ entry in tight epithelia is mediated by amiloride-inhibitable Na+ channels (1). These channels are modulated by several factors, including antidiuretic hormones, such as vasopressin. In the toad bladder and related epithelia it was demonstrated that vasopressin binds to a basolateral membrane receptor and, consequently, activates adenylate cyclase resulting in a rise in intracellular cyclic AMP (cAMP) (2). This rise brings about a two-fold increase in the number of conducting channels (3). The natriferic action of the hormone can also be mimicked by exogenous cAMP (2,4). The increase in Na+ transport was shown to be preceded by an activation of the cytosolic Type II cAMP-dependent protein kinase (cAMPPK) (5), change in cell Ca2+ (6,7), and dephosphorylation of a 50–55 KDa protein (8). This phosphoprotein was tentatively identified as the regulatory subunit of the Type II cAMPPK (9).
KeywordsRegulatory Subunit Activate Adenylate Cyclase Soybean Trypsin Inhibitor Bladder Epithelial Cell Toad Bladder
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