Feedback inhibition of epithelial Na+ channels in Xenopus oocytes does not require G0 or Gi2 proteins

FEBS Letters

Sanchez-Perez, A.²  Poronnik, P.²  Cook, D.I.²  Kunzelmann, K.²  Boucherot, A.¹  Hübner, M.¹  Schreiber, R.¹ 

[1] Physiologisches Institut, Albert-Ludwigs-Universität Freiburg, Hermann-Herder-Straße 7, 79104 Freiburg, Germany;Department of Physiology (F13), University of Sydney, Sydney, NSW 2006, Australia

关键词: Na+ feedback;    Epithelial Na+ channel;    Xenopus oocyte;    G protein;    Gi2;    G0;   

DOI  :  10.1016/S0014-5793(99)01291-0

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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 αG₀ and 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 αG₀ or 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 αG₀ had 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.

【 授权许可】

Unknown