The Dopamine Paradox in Lung and Kidney Epithelia

Bertorello, Alejandro M.; Sznajder, Jacob I.

doi:10.1165/rcmb.2005-0297tr

Cited by 52 publications

(19 citation statements)

References 55 publications

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“…In this report, we observed that when dopamine is added alone, it stimulates transcription, similar to the effects of dopamine in alveolar lung epithelial cells [57]. However, in the RPT in vivo , this stimulatory effect of dopamine may not be physiologically significant, because renal dopamine is primarily produced when Na + levels increase (which results in increased intracellular Na + in the RPT).…”

Section: Discussionmentioning

confidence: 86%

Renal proximal tubule Na,K-ATPase is controlled by CREB-regulated transcriptional coactivators as well as salt-inducible kinase 1

Taub

Garimella

Kim

et al. 2015

Cellular Signalling

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Sodium reabsorption by the kidney is regulated by locally produced natriuretic and anti-natriuretic factors, including dopamine and norepinephrine, respectively. Previous studies indicated that signaling events initiated by these natriuretic and anti-natriuretic factors achieve their effects by altering the phosphorylation of Na,K-ATPase in the renal proximal tubule, and that Protein Kinase A (PKA) and Calcium mediated signaling pathways are involved. The same signaling pathways also control the transcription of the Na,K-ATPase β subunit gene atp1b1 in renal proximal tubule cells. In this report, evidence is presented that 1) both the recently discovered cAMP-Regulated Transcriptional Coactivators (CRTCs), and Salt Inducible Kinase 1 (SIK1) contribute to the transcriptional regulation of atp1b1 in renal proximal tubule (RPT) cells, and 2) that renal effectors including norepinephrine, dopamine, prostaglandins and sodium play a role. Exogenously expressed CRTCs stimulate atp1b1 transcription. Evidence for a role of endogenous CRTCs includes the loss of transcriptional regulation of atp1b1 by a dominant negative CRTC, as well as by a CREB mutant, with an altered CRTC binding site. In a number of experimental systems, SIK phosphorylates CRTCs, which are then sequestered in the cytoplasm, preventing their nuclear effects. Consistent with such a role of SIK in primary RPT cells, atp1b1 transcription increased in the presence of a dominant negative SIK1, and in addition, regulation by dopamine, norepinephrine and monensin was disrupted by a dominant negative SIK1. These latter observations can be explained, if SIK1 is phosphorylated and inactivated in the presence of these renal effectors. Our results support the hypothesis that Na,K-ATPase in the renal proximal tubule is regulated at the transcriptional level via SIK1 and CRTCs by renal effectors, in addition to the previously reported control of the phosphorylation of Na,K-ATPase.

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Section: Discussionmentioning

confidence: 86%

Renal proximal tubule Na,K-ATPase is controlled by CREB-regulated transcriptional coactivators as well as salt-inducible kinase 1

Taub

Garimella

Kim

et al. 2015

Cellular Signalling

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“…In the basolateral membrane, D 1 -like receptors inhibit Na + /K + ATPase activity in all the nephron segments studied and electrogenic Na + /HCO 3 − co-transporter (NBCe1A, SLC4A4) in the proximal tubule (18, 27, 47, 69–72, 106, 114, 151–153, 156, 157, 186, 198, 221, 255, 322, 328, 338, 370, 438, 470, 540, 541, 556, 608). Although stimulation of D 2 -like receptors may increase Na + /K + ATPase activity (275,428,679), the interaction of D 1 -like and D 2 -like receptors results in a potentially greater inhibition of the sodium pump.…”

Section: Structure and Function Of The Renal Dopaminergic Systemmentioning

confidence: 98%

“…In the mouse kidney, the D 3 R, D 4 R, and D 5 R are most abundant in the S1 segment, while the D 1 R is most abundant in the S3 segment; the D 2 R may be mainly expressed in the S2 segment (unpublished observations). The stimulation of D 1 -like receptors decreases the activity of several sodium transporters, including the sodium hydrogen exchanger 3 (NHE3, SLC9A3) (10, 35, 167, 168, 195,196,220,271,296,471,666), sodium phosphate cotrans-porter (NaPi-IIa/SLC34A1 and NaPi-IIc/SLC34A3) (34,125, 135, 476, 661) and Cl − /HCO 3 − exchanger (SLC26A6) (472) at the apical membrane, and electrogenic Na + /HCO 3 − co-transporter (NBCe1A, SLC4A4) (338) and Na + /K + ATPase (18, 27, 47, 69–72, 106, 114, 151–153, 156, 157, 186, 198, 221, 255, 322, 328, 370, 438, 470, 540, 541, 556, 608) at the basolateral membrane. G protein-dependent, cAMP/PKA- and PKC/NHERF-1-dependent and -independent mechanisms are involved in the dopamine or D 1 -like receptor inhibition of NHE3, Na + /Pi2, and Cl − /HCO 3 − exchanger activity, including their translocation out of the brush border membranes into the cytosol (34,47,106,168,256,322,338,472,661,675).…”

Section: Structure and Function Of The Renal Dopaminergic Systemmentioning

confidence: 99%

“…Dopamine inhibits Na + /K + ATPase activity in renal tubules. However, in human ciliary non-pigmented epithelial cells, D 1 -like receptors do not affect Na + /K + ATPase activity (507) and stimulates it in pulmonary alveolar cells (72). D 2L R also stimulates Na + /K + ATPase in murine fibroblasts (679).…”

Section: Structure and Function Of The Renal Dopaminergic Systemmentioning

confidence: 99%

“…GRK2 and GRK3 phosphorylate and may aid in the internalization of Na + /K + ATPase (326). How this effect of GRK2 on D 1 R desensitization and decreased internalization of Na + /K + ATPase affects sodium transport is unclear (70,72,198,321,332,470). NKCC1 colocalizes with GRK3 in rodent olfactory epithelia but its regulation by GRK3 in the kidney has not been demonstrated (406).…”

Section: Regulation Of Dopamine Receptor Functionmentioning

confidence: 99%

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Dopamine and Renal Function and Blood Pressure Regulation

Armando

Villar

José

2011

Comprehensive Physiology

104

215

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Dopamine is an important regulator of systemic blood pressure via multiple mechanisms. It affects fluid and electrolyte balance by its actions on renal hemodynamics and epithelial ion and water transport and by regulation of hormones and humoral agents. The kidney synthesizes dopamine from circulating or filtered L-DOPA independently from innervation. The major determinants of the renal tubular synthesis/release of dopamine are probably sodium intake and intracellular sodium. Dopamine exerts its actions via two families of cell surface receptors, D1-like receptors comprising D1R and D5R, and D2-like receptors comprising D2R, D3R, and D4R, and by interactions with other G protein-coupled receptors. D1-like receptors are linked to vasodilation, while the effect of D2-like receptors on the vasculature is variable and probably dependent upon the state of nerve activity. Dopamine secreted into the tubular lumen acts mainly via D1-like receptors in an autocrine/paracrine manner to regulate ion transport in the proximal and distal nephron. These effects are mediated mainly by tubular mechanisms and augmented by hemodynamic mechanisms. The natriuretic effect of D1-like receptors is caused by inhibition of ion transport in the apical and basolateral membranes. D2-like receptors participate in the inhibition of ion transport during conditions of euvolemia and moderate volume expansion. Dopamine also controls ion transport and blood pressure by regulating the production of reactive oxygen species and the inflammatory response. Essential hypertension is associated with abnormalities in dopamine production, receptor number, and/or posttranslational modification.

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Differential Effects of Pro-Inflammatory Mediators on Alveolar Epithelial Barrier Function

Matthay

Lee

Update in Intensive Care and Emergency Medicine

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The Dopamine Paradox in Lung and Kidney Epithelia

Cited by 52 publications

References 55 publications

Renal proximal tubule Na,K-ATPase is controlled by CREB-regulated transcriptional coactivators as well as salt-inducible kinase 1

Renal proximal tubule Na,K-ATPase is controlled by CREB-regulated transcriptional coactivators as well as salt-inducible kinase 1

Dopamine and Renal Function and Blood Pressure Regulation

Differential Effects of Pro-Inflammatory Mediators on Alveolar Epithelial Barrier Function

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