ArticleAmerican journal of physiology. Renal physiology2008
Trafficking of Na-K-ATPase and dopamine receptor molecules induced by changes in intracellular sodium concentration of renal epithelial cells.
Article in American journal of physiology. Renal physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
- Genetic and genomic evidence for an important role of the NaPhysiological genomics · 2019Review
- Gene Level Regulation of Na,K-ATPase in the Renal Proximal Tubule Is Controlled by Two Independent but Interacting Regulatory Mechanisms Involving Salt Inducible Kinase 1 and CREB-Regulated Transcriptional Coactivators.International journal of molecular sciences · 2018Review
- Loss of NHERF-1 expression prevents dopamine-mediated Na-K-ATPase regulation in renal proximal tubule cells from rat models of hypertension: aged F344 rats and spontaneously hypertensive rats.American journal of physiology. Cell physiology · 2017Article
- Chronic insulin treatment phosphorylates the renal Na-K-ATPase α1-subunit at serine 16/23 and reduces its activity involving PI3-kinase-dependent PKC activation.American journal of physiology. Renal physiology · 2016Article
- Low dose ouabain stimulates NaK ATPase α1 subunit association with angiotensin II type 1 receptor in renal proximal tubule cells.Biochimica et biophysica acta · 2016Article
- Regulation of Cardiac Remodeling by Cardiac Na(+)/K(+)-ATPase Isoforms.Frontiers in physiology · 2016Review
- In vitro selection of a sodium-specific DNAzyme and its application in intracellular sensing.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- D1-like dopamine receptors downregulate Na+-K+-ATPase activity and increase cAMP production in the posterior gills of the blue crab Callinectes sapidus.American journal of physiology. Regulatory, integrative and comparative physiology · 2014Article
- Angiotensin II-induced hypertension increases plasma membrane Na pump activity by enhancing Na entry in rat thick ascending limbs.American journal of physiology. Renal physiology · 2013Article
- Proximal nephron.Comprehensive Physiology · 2013Review
- Dopamine and renal function and blood pressure regulation.Comprehensive Physiology · 2011Review
- Dopamine regulation of Na+-K+-ATPase requires the PDZ-2 domain of sodium hydrogen regulatory factor-1 (NHERF-1) in opossum kidney cells.American journal of physiology. Cell physiology · 2011Article
- Dopamine and G protein-coupled receptor kinase 4 in the kidney: role in blood pressure regulation.Biochimica et biophysica acta · 2010Review
- Ouabain stimulates Na-K-ATPase through a sodium/hydrogen exchanger-1 (NHE-1)-dependent mechanism in human kidney proximal tubule cells.American journal of physiology. Renal physiology · 2010Article
- Caveolin-1 and dopamine-mediated internalization of NaKATPase in human renal proximal tubule cells.Hypertension (Dallas, Tex. : 1979) · 2009Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Most of the transepithelial transport of sodium in proximal tubules occurs through the coordinated action of the apical sodium/proton exchanger and the basolateral Na-K-ATPase. Hormones that regulate proximal tubule sodium excretion regulate the activities of these proteins. We have previously demonstrated that the level of intracellular sodium concentration modulates the regulation of Na-K-ATPase activity by angiotensin II and dopamine. An increase of a few millimolars in intracellular sodium concentration leads to increased Na-K-ATPase activity without a statistically significant increase in the number of plasma membrane Na-K-ATPase molecules, as determined by cell surface protein biotinylation. Using total internal reflection fluorescence, we detected an increased number of Na-K-ATPase molecules in cytosolic compartments adjacent to the plasma membrane, suggesting that the increased intracellular sodium concentration induces a movement of Na-K-ATPase molecules toward the plasma membrane. While intracellular compartments containing Na-K-ATPase molecules are very close to the plasma membrane, compartments containing type 1 dopamine receptors (D1Rs) are distributed in different parts of the cell cytosol. Fluorescence determinations indicate that an increased intracellular sodium concentration induces the increased colocalization of dopamine receptors with Na-K-ATPase molecules in the region of the plasma membrane. We propose that under in vivo conditions, in response to a sodium load in the lumen of proximal tubules, an increased level of intracellular sodium in epithelial cells is an early event that triggers the cellular response that leads to dopamine inhibition of proximal tubule sodium reabsorption.
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