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This Article Full Text Full Text (PDF) All Versions of this Article: 293/4/F1238    most recent 00151.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Kim, H.-Y. Articles by Weiner, I. D. Search for Related Content PubMed PubMed Citation Articles by Kim, H.-Y. Articles by Weiner, I. D.

Effect of reduced renal mass on renal ammonia transporter family, Rh C glycoprotein and Rh B glycoprotein, expression

¹Division of Nephrology, Hypertension and Transplantation, University of Florida College of Medicine, Gainesville, Florida; ²Chungbuk National University College of Medicine, Cheongju, Korea; ³Department of Physiology, University of Florida College of Medicine, Gainesville, Florida; ⁴Department of Anatomy, Ewha Womans University, Seoul, Korea; and ⁵Nephrology and Hypertension Section, North Florida/South Georgia Veterans Health System, Gainesville, Florida

Submitted 30 March 2007 ; accepted in final form 24 July 2007

Kidneys can maintain acid-base homeostasis, despite reduced renal mass, through adaptive changes in net acid excretion, of which ammonia excretion is the predominant component. The present study examines whether these adaptations are associated with changes in the ammonia transporter family members, Rh B glycoprotein (Rhbg) and Rh C glycoprotein (Rhcg). We used normal Sprague-Dawley rats and a 5/6 ablation-infarction model of reduced renal mass; control rats underwent sham operation. After 1 wk, glomerular filtration rate, assessed as creatinine clearance, was decreased, serum bicarbonate was slightly increased, and Na⁺ and K⁺ were unchanged. Total urinary ammonia excretion was unchanged, but urinary ammonia adjusted for creatinine clearance, an index of per nephron ammonia metabolism, increased significantly. Although reduced renal mass did not alter total Rhcg protein expression, both light microscopy and immunohistochemistry with quantitative morphometric analysis demonstrated hypertrophy of both intercalated cells and principal cells in the cortical and outer medullary collecting duct that was associated with increased apical and basolateral Rhcg polarization. Rhbg expression, analyzed using immunoblot analysis, immunohistochemistry, and measurement of cell-specific expression, was unchanged. We conclude that altered subcellular localization of Rhcg contributes to adaptive changes in single-nephron ammonia metabolism and maintenance of acid-base homeostasis in response to reduced renal mass.

intercalated cell; principal cell; cortical collecting duct; outer medullary collecting duct