Na(+)-H(+) exchange in salivary secretory cells is controlled by an intracellular Na(+) receptor.

Abstract:

:It recently has been shown that epithelial Na(+) channels are controlled by a receptor for intracellular Na(+), a G protein (G(o)), and a ubiquitin-protein ligase (Nedd4). Furthermore, mutations in the epithelial Na(+) channel that underlie the autosomal dominant form of hypertension known as Liddle's syndrome inhibit feedback control of Na(+) channels by intracellular Na(+). Because all epithelia, including those such as secretory epithelia, which do not express Na(+) channels, need to maintain a stable cytosolic Na(+) concentration ([Na(+)](i)) despite fluctuating rates of transepithelial Na(+) transport, these discoveries raise the question of whether other Na(+) transporting systems in epithelia also may be regulated by this feedback pathway. Here we show in mouse mandibular secretory (endpiece) cells that the Na(+)-H(+) exchanger, NHE1, which provides a major pathway for Na(+) transport in salivary secretory cells, is inhibited by raised [Na(+)](i) acting via a Na(+) receptor and G(o). This inhibition involves ubiquitination, but does not involve the ubiquitin protein ligase, Nedd4. We conclude that control of membrane transport systems by intracellular Na(+) receptors may provide a general mechanism for regulating intracellular Na(+) concentration.

authors

Ishibashi H,Dinudom A,Harvey KF,Kumar S,Young JA,Cook DI

doi

10.1073/pnas.96.17.9949

keywords:

subject

Has Abstract

pub_date

1999-08-17 00:00:00

pages

9949-53

issue

17

eissn

0027-8424

issn

1091-6490

journal_volume

96

pub_type

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