ArticleAmerican journal of physiology. Renal physiology2014
Effect of collecting duct-specific deletion of both Rh B Glycoprotein (Rhbg) and Rh C Glycoprotein (Rhcg) on renal response to metabolic acidosis.
Article in American journal of physiology. Renal physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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35 citing papers in PubMed, 41 citations in OpenAlex.
- Sex differences in renal acid-base regulation.Current opinion in nephrology and hypertension · 2026Review
- Uncoupling proximal tubule ammoniagenesis from bicarbonate generation byAmerican journal of physiology. Renal physiology · 2026Article
- Effects of proximal tubule NBCe1-A deletion on collecting duct intercalated cell responses to hypokalemia.American journal of physiology. Renal physiology · 2026Article
- Mutations in ammonia transporter RhBG that impair NHThe Journal of physiology · 2026Article
- Ammonia transport mediated by urea transporter A isoforms.Biology open · 2025Article
- Lack of a role of NHE4 in renal ammonia metabolism.American journal of physiology. Renal physiology · 2025Article
- Role of KThe American journal of pathology · 2025Article
- State of knowledge on ammonia handling by the kidney.Pflugers Archiv : European journal of physiology · 2024Review
- Mechanisms and physiological relevance of acid-base exchange in functional units of the kidney.PeerJ · 2024Review
- High dietary KAmerican journal of physiology. Renal physiology · 2023Article
- The proximal tubule through an NBCe1-dependent mechanism regulates collecting duct phenotypic and remodeling responses to acidosis.American journal of physiology. Renal physiology · 2023Article
- Acid-base effects of combined renal deletion of NBCe1-A and NBCe1-B.American journal of physiology. Renal physiology · 2022Article
- Role of the renal androgen receptor in sex differences in ammonia metabolism.American journal of physiology. Renal physiology · 2021Article
- Regulation of Rhcg, an ammonia transporter, by aldosterone in the kidney.The Journal of endocrinology · 2021Article
- Testosterone modulates renal ammonia metabolism.American journal of physiology. Renal physiology · 2020Article
- NBCe1-A is required for the renal ammonia and KAmerican journal of physiology. Renal physiology · 2020Article
- Differences in acidosis-stimulated renal ammonia metabolism in the male and female kidney.American journal of physiology. Renal physiology · 2019Article
- Regulation of renal NaDC1 expression and citrate excretion by NBCe1-A.American journal of physiology. Renal physiology · 2019Article
- Emerging Features of Ammonia Metabolism and Transport in Acid-Base Balance.Seminars in nephrology · 2019Review
- Expression of the B splice variant of NBCe1 (SLC4A4) in the mouse kidney.American journal of physiology. Renal physiology · 2018Article
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5 authors at 4 institutions in 2 countries.
Funding
Abstract
The Rhesus (Rh) glycoproteins, Rh B and Rh C Glycoprotein (Rhbg and Rhcg, respectively), are ammonia-specific transporters expressed in renal distal nephron and collecting duct sites that are necessary for normal rates of ammonia excretion. The purpose of the current studies was to determine the effect of their combined deletion from the renal collecting duct (CD-Rhbg/Rhcg-KO) on basal and acidosis-stimulated acid-base homeostasis. Under basal conditions, urine pH and ammonia excretion and serum HCO3(-) were similar in control (C) and CD-Rhbg/Rhcg-KO mice. After acid-loading for 7 days, CD-Rhbg/Rhcg-KO mice developed significantly more severe metabolic acidosis than did C mice. Acid loading increased ammonia excretion, but ammonia excretion increased more slowly in CD-Rhbg/Rhcg-KO and it was significantly less than in C mice on days 1-5. Urine pH was significantly more acidic in CD-Rhbg/Rhcg-KO mice on days 1, 3, and 5 of acid loading. Metabolic acidosis increased phosphenolpyruvate carboxykinase (PEPCK) and Na(+)/H(+) exchanger NHE-3 and decreased glutamine synthetase (GS) expression in both genotypes, and these changes were significantly greater in CD-Rhbg/Rhcg-KO than in C mice. We conclude that 1) Rhbg and Rhcg are critically important in the renal response to metabolic acidosis; 2) the significantly greater changes in PEPCK, NHE-3, and GS expression in acid-loaded CD-Rhbg/Rhcg-KO compared with acid-loaded C mice cause the role of Rhbg and Rhcg to be underestimated quantitatively; and 3) in mice with intact Rhbg and Rhcg expression, metabolic acidosis does not induce maximal changes in PEPCK, NHE-3, and GS expression despite the presence of persistent metabolic acidosis.
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