ArticleThe Journal of physiology2001
Profiling of renal tubule Na+ transporter abundances in NHE3 and NCC null mice using targeted proteomics.
Article in The Journal of physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 107 citations in OpenAlex.
- Downloadable tool for modeling of salt, urea, and water transport in a renal tubule segment: application to the DCT.American journal of physiology. Renal physiology · 2025Article
- Genetic deletion of the kidney sodium/proton exchanger-3 (NHE3) does not alter calcium and phosphate balance due to compensatory responses.Kidney international · 2025Article
- Kidney and blood pressure regulation-latest evidence for molecular mechanisms.Clinical kidney journal · 2023Review
- The NaFrontiers in physiology · 2022Review
- Circadian Control of Sodium and Blood Pressure Regulation.American journal of hypertension · 2021Review
- Regulatory control of the Na-Cl co-transporter NCC and its therapeutic potential for hypertension.Acta pharmaceutica Sinica. B · 2021Review
- Regulation of renal Na transporters in response to dietary K.American journal of physiology. Renal physiology · 2018Article
- Differential roles of WNK4 in regulation of NCC in vivo.American journal of physiology. Renal physiology · 2018Article
- Renal tubular NHE3 is required in the maintenance of water and sodium chloride homeostasis.Kidney international · 2017Article
- Acetazolamide Attenuates Lithium-Induced Nephrogenic Diabetes Insipidus.Journal of the American Society of Nephrology : JASN · 2016Article
- The CUL3/KLHL3-WNK-SPAK/OSR1 pathway as a target for antihypertensive therapy.American journal of physiology. Renal physiology · 2016Article
- Article
- Azilsartan Improves Salt Sensitivity by Modulating the Proximal Tubular Na+-H+ Exchanger-3 in Mice.PloS one · 2016Article
- ANG II-induced hypertension in the VCD mouse model of menopause is prevented by estrogen replacement during perimenopause.American journal of physiology. Regulatory, integrative and comparative physiology · 2015Article
- Development of a rat model of D-galactosamine/lipopolysaccharide induced hepatorenal syndrome.World journal of gastroenterology · 2015Article
- Caffeine-induced diuresis and natriuresis is independent of renal tubular NHE3.American journal of physiology. Renal physiology · 2015Article
- Integrated compensatory network is activated in the absence of NCC phosphorylation.The Journal of clinical investigation · 2015Article
- Renal NHE expression and activity in neonatal NHE3- and NHE8-null mice.American journal of physiology. Renal physiology · 2015Article
- Article
- Protein phosphatase 1 inhibitor-1 deficiency reduces phosphorylation of renal NaCl cotransporter and causes arterial hypotension.Journal of the American Society of Nephrology : JASN · 2014Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The Na+-H+ exchanger NHE3 and the thiazide-sensitive Na+-Cl- cotransporter NCC are the major apical sodium transporters in the proximal convoluted tubule and the distal convoluted tubule of the kidney, respectively. We investigated the mechanism of compensation that allows maintenance of sodium balance in NHE3 knockout mice and in NCC knockout mice. We used a so-called 'targeted proteomics' approach, which profiles the entire renal tubule with regard to changes in Na+ transporter and aquaporin abundance in response to the gene deletions. Specific antibodies to the Na+ transporters and aquaporins expressed along the nephron were utilized to determine the relative abundance of each transporter. Semiquantitative immunoblotting was used which gives an estimate of the percentage change in abundance of each transporter in knockout compared with wild-type mice. In NHE3 knockout mice three changes were identified which could compensate for the loss of NHE3-mediated sodium absorption. (a) The proximal sodium-phosphate cotransporter NaPi-2 was markedly upregulated. (b) In the collecting duct, the 70 kDa form of the y-subunit of the epithelial sodium channel, ENaC, exhibited an increase in abundance. This is thought to be an aldosterone-stimulated form of y-ENaC. (c) Glomerular filtration was significantly reduced. In the NCC knockout mice, amongst all the sodium transporters expressed along the renal tubule, only the 70 kDa form of the y-subunit of the epithelial sodium channel, ENaC, exhibited an increase in abundance. In conclusion, both mouse knockout models demonstrated successful compensation for loss of the deleted transporter. More extensive adaptation occurred in the case of the NHE3 knockout, presumably because NHE3 is responsible for much more sodium absorption in normal mice than in NCC knockout mice.
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