Locally formed dopamine modulates renal Na-Pi co-transport through DA1 and DA2 receptors

Perrichot, Régine; Garcı́a-Ocaña, Adolfo; Couette, Sylviane; Comoy, E; Amiel, Catherine; Friedlander, Gérard

doi:10.1042/bj3120433

Cited by 41 publications

(22 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…7 Moreover, in concert with a D 1 -like agonist, a D 2 -like agonist acts synergistically to inhibit Na ϩ -K ϩ -ATPase and sodium hydrogen exchanger activity in RPT cells and brain striatal cells and sodium-phosphate cotransport activity in opossum kidney cells. [3][4][5] The Our studies show that in the maximally vasorelaxed mesenteric artery, a D 1 receptor agonist (fenoldopam) or a D 3 receptor agonist, PD128907, a 120-fold selectivity over the D 2 receptor 26 has no effect on vascular contractility, in agreement with our previous report. 23 The current studies also support our previous report of the vasorelaxant effect of D 1 or D 3 receptors; D 1 -like receptor-induced vasorelaxation is increased with D 3 receptor activation in WKY rats.…”

Section: Discussionsupporting

confidence: 81%

“…In vitro studies have shown that a D 2 -like receptor, in concert with a D 1 -like receptor, synergistically decreases Na ϩ -K ϩ -ATPase, sodium-phosphate co-transporter, and sodium hydrogen exchanger activities in renal proximal tubule and other cells. [3][4][5] In rats, during conditions of normal sodium load, and especially with increased sodium load, D 1 -like and D 2 -like receptors interact to increase sodium excretion. 1,2,6,7 The D 1 -like receptor interacting with the specific D 2 -like receptor subtype in renal sodium transport is unknown.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Aberrant D ₁ and D ₃ Dopamine Receptor Transregulation in Hypertension

Zeng

Wang²,

Asico³

et al. 2004

Hypertension

View full text Add to dashboard Cite

Abstract-Dopamine plays a role in the regulation of blood pressure by inhibition of sodium transport in renal proximal tubules (RPTs) and relaxation of vascular smooth muscles. Key Words: receptors Ⅲ dopamine Ⅲ rats Ⅲ hypertension Ⅲ normotension Ⅲ kidney Ⅲ vascular smooth muscle S everal studies have reported that an impaired renal dopaminergic system may contribute to the pathogenesis of hypertension. 1,2 There is increasing evidence for a direct interaction between D 1 -like and D 2 -like receptors in the kidney. In vitro studies have shown that a D 2 -like receptor, in concert with a D 1 -like receptor, synergistically decreases Na ϩ -K ϩ -ATPase, sodium-phosphate co-transporter, and sodium hydrogen exchanger activities in renal proximal tubule and other cells. [3][4][5] In rats, during conditions of normal sodium load, and especially with increased sodium load, D 1 -like and D 2 -like receptors interact to increase sodium excretion. 1,2,6,7 The D 1 -like receptor interacting with the specific D 2 -like receptor subtype in renal sodium transport is unknown. The 12 We have found that these immortalized RPT cells have characteristics similar to freshly obtained RPTs and RPT brush-border membranes, at least regarding D 1 -like receptors and responses to G-protein stimulation. [13][14][15] The present studies were designed to determine whether D 1 -like receptors regulate D 1 and D 3 receptors and whether the regulation is different in RPT cells from WKY rats and spontaneously hypertensive rats (SHRs).

show abstract

Section: Discussionsupporting

confidence: 81%

mentioning

confidence: 99%

Aberrant D ₁ and D ₃ Dopamine Receptor Transregulation in Hypertension

Zeng

Wang²,

Asico³

et al. 2004

Hypertension

View full text Add to dashboard Cite

show abstract

“…In the proximal tubule where 50 -60% of NaCl and water is reabsorbed, DA inhibits the basolateral membrane Na ϩ ,K ϩ -ATPase (34 -38), which is the primary driving force for transepithelial Na ϩ absorption. In addition, DA also inhibits two apical Na ϩ -coupled transporters, the Na ϩ -coupled inorganic phosphate transporter (92)(93)(94)(95)(96)) and the Na ϩ /H ϩ exchanger NHE3 (27)(28)(29)(30)(31)(32)(33). In addition to transcellular Na ϩ flux, inhibition of NHE3 also reduces the driving force for paracellular NaCl transport (97).…”

Section: Discussionmentioning

confidence: 99%

Dopamine Acutely Stimulates Na+/H+Exchanger (NHE3) Endocytosis via Clathrin-coated Vesicles

Hu¹,

Fan²,

Crowder³

et al. 2001

Journal of Biological Chemistry

138

167

View full text Add to dashboard Cite

Extracellular fluid volume and to a certain extent blood pressure in mammals are determined by the balance between sodium intake and renal sodium excretion (1, 2). As regulator of sodium excretion, the intrarenal autocrine-paracrine dopamine (DA) 1 system assumes far greater importance than circulating endocrine or neurogenic dopamine (3-6). DA is produced in the proximal tubule via decarboxylation of its precursor L-dihydroxyphenylalanine derived from the plasma and glomerular filtrate (7-9) and is then secreted into the tubular lumen where it exerts its effects on multiple nephron segments, which cumulates in inhibition of tubular sodium absorption and natriuresis. Renal DA synthesis and excretion are increased by increased dietary salt and an intravenous saline load (10 -13), and blockade of DA synthesis or DA receptor significantly blunts the natriuretic response (14 -18). Quantitatively, the most significant inhibition of sodium transport occurs in the proximal tubule. DA inhibits proximal tubule sodium absorption partially by hemodynamic alterations (19 -22), but the major effect is directly on the tubule epithelium (23-26) via inhibition of two principal sodium transporters: the apical membrane Na ϩ /K ϩ exchanger (NHE3) (27-33) and the basolateral Na ϩ ,K ϩ -ATPase (34 -38). These effects are mediated by the DA receptor where five molecular isoforms (DR 1 -like receptors: DR 1 and DR 5 , and DR 2 -like receptors DR 2 , DR 3 , and DR 4 ) have been identified to date; all five isoforms are known to be present in the renal tubular epithelium (39 -43).Previous studies in isolated apical membrane vesicles have shown that DA inhibits proximal tubule apical membrane Na ϩ /H ϩ exchange activity mainly via DR 1 -like receptors (25-28, 30, 31, 33) through both PKA-dependent and PKA-independent mechanisms (27, 31). The Na ϩ /H ϩ exchanger on the apical membrane of the renal proximal tubule is encoded by NHE3 (44 -46), one of the seven members of the NHE gene family (47). We have shown in opossum kidney (OK) cells that the DA 1 -like and DA 2 -like receptors have synergistic actions on NHE3 activity and that inhibition of NHE3 activity by DA is accompanied by complex changes in NHE3 phosphorylation and dephosphorylation (33). However, the mechanisms by which DA acutely reduces NHE3 activity have not been examined. Redistribution of NHE3 transporters has been shown to mediate regulation of NHE3 activity in intact kidney (48 -54), in cultured renal epithelial cells (55,56), and in transfected fibroblasts (57-64). In addition, although NHE phosphorylation has been associated with changes in NHE3 activity (52,(65)(66)(67)(68), and phosphorylation appears to be functionally important for regulation of NHE3 activity by pharmacologic activators of protein kinases in transfected fibroblasts (65-67), the physiologic significance of NHE3 phosphorylation is still undetermined. In this paper we characterize one mechanism by which DA acutely inhibits NHE3: the internalization of NHE3 secondary to PKA-mediated NHE3 phosphorylatio...

show abstract

“…Although no flux measurements have been made in the collecting duct, DA inhibits Na ϩ -K ϩ -ATPase in this segment, which is expected to decrease transepithelial Na ϩ absorption (101). In the proximal tubule where the most significant quantity of Na ϩ absorption occurs, DA decreases Na ϩ flux (18,20) by inhibiting three Na ϩ transporters: the Na ϩ /H ϩ exchanger-3 (NHE3) (2,12,36,39,59,92,108,109) and Na ϩ -phosphate cotransporter -IIa (NaPi-IIa) (11,13,42,72,85) on the apical membrane, and the Na ϩ -K ϩ -ATPase on the basolateral membrane (8,21,22). In the mammalian renal proximal tubule, the synthesis, metabolism, release, and target action of dopamine all take place in the same cells, thus constituting a genuine self-sufficient autocrine-paracrine natriuretic system.…”

mentioning

confidence: 99%

Chronic regulation of the renal Na⁺/H⁺exchanger NHE3 by dopamine: translational and posttranslational mechanisms

Sole

Zhang

et al. 2013

American Journal of Physiology-Renal Physiology

View full text Add to dashboard Cite

The intrarenal autocrine/paracrine dopamine (DA) system contributes to natriuresis in response to both acute and chronic Na+ loads. While the acute DA effect is well described, how DA induces natriuresis chronically is not known. We used an animal and a cell culture model to study the chronic effect of DA on a principal renal Na+ transporter, Na+/H+ exchanger-3 (NHE3). Intraperitoneal injection of Gludopa in rats for 2 days elevated DA excretion and decreased total renal cortical and apical brush-border NHE3 antigen. Chronic treatment of an opossum renal proximal cell line with DA decreased NHE3 activity, cell surface and total cellular NHE3 antigen, but not NHE3 transcript. The decrease in NHE3 antigen was dose and time dependent with maximal inhibition at 16–24 h and half maximal effect at 3 × 10−7 M. This is in contradistinction to the acute effect of DA on NHE3 (half maximal at 2 × 10−6 M), which was not associated with changes in total cellular NHE3 protein. The DA-induced decrease in total NHE3 protein was associated with decrease in NHE3 translation and mediated by cis-sequences in the NHE3 5′-untranslated region. DA also decreased cell surface and total cellular NHE3 protein half-life. The DA-induced decrease in total cellular NHE3 was partially blocked by proteasome inhibition but not by lysosome inhibition, and DA increased ubiquitylation of total and surface NHE3. In summary, chronic DA inhibits NHE3 with mechanisms distinct from its acute action and involves decreased NHE3 translation and increased NHE3 degradation, which are novel mechanisms for NHE3 regulation.

show abstract

Locally formed dopamine modulates renal Na-Pi co-transport through DA1 and DA2 receptors

Cited by 41 publications

References 42 publications

Aberrant D ₁ and D ₃ Dopamine Receptor Transregulation in Hypertension

Aberrant D ₁ and D ₃ Dopamine Receptor Transregulation in Hypertension

Dopamine Acutely Stimulates Na+/H+Exchanger (NHE3) Endocytosis via Clathrin-coated Vesicles

Chronic regulation of the renal Na⁺/H⁺exchanger NHE3 by dopamine: translational and posttranslational mechanisms

Contact Info

Product

Resources

About

Locally formed dopamine modulates renal Na-Pi co-transport through DA1 and DA2 receptors

Cited by 41 publications

References 42 publications

Aberrant D 1 and D 3 Dopamine Receptor Transregulation in Hypertension

Aberrant D 1 and D 3 Dopamine Receptor Transregulation in Hypertension

Dopamine Acutely Stimulates Na+/H+Exchanger (NHE3) Endocytosis via Clathrin-coated Vesicles

Chronic regulation of the renal Na+/H+exchanger NHE3 by dopamine: translational and posttranslational mechanisms

Contact Info

Product

Resources

About

Aberrant D ₁ and D ₃ Dopamine Receptor Transregulation in Hypertension

Aberrant D ₁ and D ₃ Dopamine Receptor Transregulation in Hypertension

Chronic regulation of the renal Na⁺/H⁺exchanger NHE3 by dopamine: translational and posttranslational mechanisms