Regulation of amiloride-sensitive epithelial Na+channels (ENaC) is a prerequisite for coordination of electrolyte transport in epithelia. Downregulation of Na+conductance occurs when the intracellular Na+concentration is increased during reabsorption of electrolytes, known as feedback inhibition. Recent studies have demonstrated the involvement of αG0and αG(i2) proteins in the feedback control of ENaC in mouse salivary duct cells. In this report, we demonstrate that Na+feedback inhibition is also present in Xenopus oocytes after expression of rat α,β,γ-ENaC. Interfering with intracellular αG0or αG(i2) signaling by coexpression of either constitutively active αG0/αG(i2) or dominant negative αG0/αG(i2) and by coinjecting sense or antisense oligonucleotides for αG0had no impact on Na+feedback. Moreover, no evidence for involvement of the intracellular G protein cascade was found in experiments in which a regulator of G protein signaling (RGS3) or β-adrenergic receptor kinase (βARK) was coexpressed together with α,β,γ-ENaC. Although some experiments suggest the presence of an intracellular Na+receptor, we may conclude that Na+feedback in Xenopus oocytes is different from that described for salivary duct cells in that it does not require G protein signaling. Copyright (C) 1999 Federation of European Biochemical Societies.
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