Changes in subcellular distribution of the ammonia transporter, Rhcg, in response to chronic metabolic acidosis.

@article{Seshadri2006ChangesIS,
  title={Changes in subcellular distribution of the ammonia transporter, Rhcg, in response to chronic metabolic acidosis.},
  author={Ramanathan M. Seshadri and Janet D. Klein and Tekla D Smith and Jeff M. Sands and Mary E. Handlogten and Jill W. Verlander and I. David Weiner},
  journal={American journal of physiology. Renal physiology},
  year={2006},
  volume={290 6},
  pages={
          F1443-52
        }
}
The primary mechanism by which the kidneys mediate net acid excretion is through ammonia metabolism. In the current study, we examined whether chronic metabolic acidosis, which increases ammonia metabolism, alters the cell-specific and/or the subcellular expression of the ammonia transporter family member, Rhcg, in the outer medullary collecting duct in the inner stripe (OMCDi). Chronic metabolic acidosis was induced in normal SD rats by HCl ingestion for 7 days; controls were pair-fed. The… 
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Basolateral expression of the ammonia transporter family member Rh C glycoprotein in the mouse kidney.
TLDR
It is concluded that Rhcg is present in both the apical and basolateral plasma membrane in the mouse kidney, where it is likely to contribute to renal ammonia metabolism.
Expression of the ammonia transporter, rh C glycoprotein, in normal and neoplastic human kidney.
TLDR
The studies suggest that RhCG contributes to both apical and basolateral membrane ammonia transport in the human kidney.
The role of the renal ammonia transporter Rhcg in metabolic responses to dietary protein.
TLDR
The renal adaptive response of acid excretory pathways in mice to high-protein diets containing normal or low amounts of acid-producing sulfur amino acids (SAA) is investigated and how this adaption requires the RhCG ammonia transporter is examined.
Effect of hypokalemia on renal expression of the ammonia transporter family members, Rh B Glycoprotein and Rh C Glycoprotein, in the rat kidney.
TLDR
It is concluded that in rat OMCD, hypokalemia increases Rhcg expression, causes more polarized apical expression in intercalated cells, and increases both apical and basolateral expression in the principal cell.
Molecular physiology of the Rh ammonia transport proteins
TLDR
No longer can NH3 transport be considered to occur only through diffusive NH3 movement, asTransporter-mediated NH2 movement is fundamental to ammonia metabolism, and the role of Rh glycoproteins in renal ammonia transport is summarized.
Role of the Rhesus glycoprotein, Rh B glycoprotein, in renal ammonia excretion.
TLDR
It is concluded that intercalated cell Rhbg contributes to acidosis-stimulated renal ammonia excretion, Rhbg in CNT and principal cells may contribute to renal ammoniaexcretion, and decreased glutamine synthetase expression may enable normal rates of ammonia excrete under both basal conditions and on day 5 of acid loading in IC-Rhbg-KO mice.
Expression of the non-erythroid Rh glycoproteins in mammalian tissues.
  • I. Weiner
  • Biology
    Transfusion clinique et biologique : journal de la Societe francaise de transfusion sanguine
  • 2006
Renal ammonia excretion in response to hypokalemia: effect of collecting duct-specific Rh C glycoprotein deletion.
TLDR
It is concluded that hypokalemia increases collecting duct Rhcg expression, that this likely contributes to the hypkalemia-stimulated increase in urinary ammonia excretion, and that adaptive increases in PDG expression can compensate for the absence of collecting ductRhcg.
Effect of intercalated cell-specific Rh C glycoprotein deletion on basal and metabolic acidosis-stimulated renal ammonia excretion.
TLDR
Rhcg expression in intercalated cells is necessary for the normal renal response to metabolic acidosis; principal cell Rhcg contributes to both basal and acidosis-stimulated ammonia excretion; and adaptations in Rhbg expression occur in response to acid-loading.
Intercalated cell-specific Rh B glycoprotein deletion diminishes renal ammonia excretion response to hypokalemia.
TLDR
It is concluded that hypokalemia increases Rhbg expression in intercalated cells in the cortex and outer medulla and that interCalated cell RhBG expression is necessary for the normal increase in renal ammonia excretion in response to hypokAlemia.
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