ArticleAmerican journal of physiology. Renal physiology2009
Collecting duct-specific Rh C glycoprotein deletion alters basal and acidosis-stimulated renal ammonia excretion.
Article in American journal of physiology. Renal physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
69 citing papers in PubMed, 95 citations in OpenAlex.
- Uncoupling proximal tubule ammoniagenesis from bicarbonate generation byAmerican journal of physiology. Renal physiology · 2026Article
- Sex differences in renal acid-base regulation.Current opinion in nephrology and hypertension · 2026Review
- Effects of proximal tubule NBCe1-A deletion on collecting duct intercalated cell responses to hypokalemia.American journal of physiology. Renal physiology · 2026Article
- Ammonia transport mediated by urea transporter A isoforms.Biology open · 2025Article
- Collecting duct NCOR1 controls blood pressure by regulating mineralocorticoid receptor.Journal of advanced research · 2025Article
- Role of KThe American journal of pathology · 2025Article
- Article
- State of knowledge on ammonia handling by the kidney.Pflugers Archiv : European journal of physiology · 2024Review
- A Novel Form of Renal Tubular Acidosis Associated With Immune Checkpoint Inhibitors.Kidney international reports · 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
- NBCe1-B/C-knockout mice exhibit an impaired respiratory response and an enhanced renal response to metabolic acidosis.Frontiers in physiology · 2023Article
- Ammonium chloride-induced acidosis exacerbates cystitis and pyelonephritis caused by uropathogenic E. coli.Physiological reports · 2022Article
- Acid-base effects of combined renal deletion of NBCe1-A and NBCe1-B.American journal of physiology. Renal physiology · 2022Article
- A Deep Insight Into Regulatory T Cell Metabolism in Renal Disease: Facts and Perspectives.Frontiers in immunology · 2022Review
- 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
- Effects of chronic hypercapnia on ammonium transport in the mouse kidney.Physiological reports · 2019Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
NH3 movement across plasma membranes has traditionally been ascribed to passive, lipid-phase diffusion. However, ammonia-specific transporters, Mep/Amt proteins, are present in primitive organisms and mammals express orthologs of Mep/Amt proteins, the Rh glycoproteins. These findings suggest that the mechanisms of NH3 movement in mammalian tissues should be reexamined. Rh C glycoprotein (Rhcg) is expressed in the collecting duct, where NH3 secretion is necessary for both basal and acidosis-stimulated ammonia transport. To determine whether the collecting duct secretes NH3 via Rhcg or via lipid-phase diffusion, we generated mice with collecting duct-specific Rhcg deletion (CD-KO). CD-KO mice had loxP sites flanking exons 5 and 9 of the Rhcg gene (Rhcg(fl/fl)) and expressed Cre-recombinase under control of the Ksp-cadherin promoter (Ksp-Cre). Control (C) mice were Rhcg(fl/fl) but Ksp-Cre negative. We confirmed kidney-specific genomic recombination using PCR analysis and collecting duct-specific Rhcg deletion using immunohistochemistry. Under basal conditions, urinary ammonia excretion was less in KO vs. C mice; urine pH was unchanged. After acid-loading for 7 days, CD-KO mice developed more severe metabolic acidosis than did C mice. Urinary ammonia excretion did not increase significantly on the first day of acidosis in CD-KO mice, despite an intact ability to increase urine acidification, whereas it increased significantly in C mice. On subsequent days, urinary ammonia excretion slowly increased in CD-KO mice, but was always significantly less than in C mice. We conclude that collecting duct Rhcg expression contributes to both basal and acidosis-stimulated renal ammonia excretion, indicating that collecting duct ammonia secretion is, at least in part, mediated by Rhcg and not solely by lipid diffusion.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.