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Background  It was previously shown that K +  secretion by strial marginal cell epithelium is under the control of G-protein coupled receptors of the P2Y family in the apical membrane. Receptor activation by uracil nucleotides (P2Y 2 , P2Y 4  or P2Y 6 ) leads to a decrease in the electrogenic K +  secretion. The present study was conducted to determine the subtype of the functional purinergic receptor in gerbil stria vascularis, to test if receptor activation leads to elevation of intracellular [Ca 2+ ] and to test if the response to these receptors undergoes desensitization.    Results  The transepithelial short circuit current (Isc) represents electrogenic K +  secretion and was found to be decreased by uridine 5'-triphosphate (UTP), adenosine 5'-triphosphate (ATP) and diadenosine tetraphosphate (Ap4A) but not uridine 5'-diphosphate (UDP) at the apical membrane of marginal cells of the gerbil stria vascularis. The potencies of these agonists were consistent with rodent P2Y 4  and P2Y 2  but not P2Y 6  receptors. Activation caused a biphasic increase in intracellular [Ca 2+ ] that could be partially blocked by 2-aminoethoxy-diphenyl borate (2-APB), an inhibitor of the IP3 receptor and store-operated channels. Suramin (100 μM) did not inhibit the effect of UTP (1 μM). The ineffectiveness of suramin at the concentration used was consistent with P2Y 4  but not P2Y 2 . Transcripts for both P2Y 2  and P2Y 4  were found in the stria vascularis. Sustained exposure to ATP or UTP for 15 min caused a depression of Isc that appeared to have two components but with apparently no chronic desensitization.    Conclusion  The results support the conclusion that regulation of K +  secretion across strial marginal cell epithelium occurs by P2Y 4  receptors at the apical membrane. The apparent lack of desensitization of the response is consistent with two processes: a rapid-onset phosphorylation of KCNE1 channel subunit and a slower-onset of regulation by depletion of plasma membrane PIP 2 .

Apical membrane P2Y4 purinergic receptor controls K+ secretion by strial marginal cell epithelium