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J. Biol. Chem., Vol. 276, Issue 29, 26906-26915, July 20, 2001
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From the ¶ Medical Service, Department of Veterans Affairs
Medical Center, Dallas, Texas 75216, the Dopamine (DA) is a key hormone in
mammalian sodium homeostasis. DA induces natriuresis via acute
inhibition of the renal proximal tubule apical membrane
Na+/H+ exchanger NHE3. We examined
the mechanism by which DA inhibits NHE3 in a renal cell line. DA
acutely decreases surface NHE3 antigen in dose- and
time-dependent fashion without altering total cellular NHE3. Although DA1 receptor agonist alone decreases surface
NHE3, simultaneous DA2 agonist synergistically enhances the
effect of DA1. Decreased surface NHE3 antigen, caused by
stimulation of NHE3 endocytosis, is dependent on intact functioning of
the GTPase dynamin and involves increased binding of NHE3 to the
adaptor protein AP2. DA-stimulated NHE3 endocytosis can be blocked by pharmacologic or genetic protein kinase A inhibition or by mutation of
two protein kinase A target serines (Ser-560 and Ser-613) on NHE3. We
conclude that one mechanism by which DA induces natriuresis is via
protein kinase A-mediated phosphorylation of proximal tubule NHE3
leading to endocytosis of NHE3 via clathrin-coated vesicles.
Dopamine Acutely Stimulates Na+/H+
Exchanger (NHE3) Endocytosis via Clathrin-coated Vesicles
DEPENDENCE ON PROTEIN KINASE A-MEDIATED NHE3
PHOSPHORYLATION*
,,,¶
Department of
Internal Medicine, University of Texas Southwestern Medical Center,
Dallas, Texas 75390-8856, and the § Institute of Physiology,
University of Zürich, Zürich 8057, Switzerland
*
This work was supported by National Institutes of Health
Grants DK-48482 and DK-54396 (to O. W. M.), by the Department of Veterans Affairs Research Service (to O. W. M.), American Heart Association Texas Affiliate Grant 98G-052 (to O. W. M.), and Swiss National Science Foundation Grant 3100-46523.96 (to H. M.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Dept. of Internal
Medicine, University of Texas Southwestern Medical Center, 5323 Harry
Hines Blvd., Dallas, TX 75390-8856. Tel.: 214-648-3152; Fax:
214-648-2071; E-mail: orson.moe@utsouthwestern.edu.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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