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1 Division of Nephrology, Hypertension and Transplantation, University of Florida College of Medicine, Gainesville, Florida, United States; College of Medicine, Chungbuk National University, Cheongju, Korea, Republic of
2 Physiology and Functional Genomics, University of Florida, Gainesville, Florida, United States
3 Division of Nephrology, Hypertension and Transplantation, University of Florida, Gainesville, Florida, United States
4 Anatomy, Ewha Womans University, Seoul, Korea, Republic of
5 Division of Nephrology, Hypertension and Transplantation, University of Florida College of Medicine, Gainesville, Florida, United States
6 Div. of Nephrol., Hypertension & Transplant., Univ. of Fla. College of Medicine, P.O. Box 100224, Gainsville, Florida, 32610, United States
7 Nephrology and Hypertension Section, NF/SGVHS, Gainesville, Florida, United States; Div. of Nephrol., Hypertension & Transplant., Univ. of Fla. College of Medicine, P.O. Box 100224, Gainsville, Florida, 32610, United States
* To whom correspondence should be addressed. E-mail: weineid{at}ufl.edu.
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 current study examines whether these adaptations are associated with changes in the ammonia transporter family members, Rhbg and Rhcg. We used normal Sprague-Dawley rats and a 5/6 ablation-infarction model of reduced renal mass; control rats underwent sham operation. After one week, GFR, assessed as creatinine clearance (ClCr), was decreased, serum bicarbonate was slightly increased and Na+ and K+ were unchanged. Total urinary ammonia excretion was unchanged, but urinary ammonia adjusted for ClCr, 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.
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