Effect of reduced renal mass on renal ammonia transporter family, Rh C glycoprotein and Rh B glycoprotein, expression.
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.
Kim
Hye-Young
HY
Division of Nephrology, Hypertension and Transplantation, University of Florida College of Medicine, Gainesville, Florida, USA.
Baylis
Chris
C
Verlander
Jill W
JW
Han
Ki-Hwan
KH
Reungjui
Sirirat
S
Handlogten
Mary E
ME
Weiner
I David
ID
D000136:Acid-Base Equilibrium / Q000502:physiology; D000641:Ammonia / Q000378:metabolism*; D000818:Animals; D017115:Catheter Ablation; D027682:Cation Transport Proteins / Q000378:metabolism*; D006706:Homeostasis / Q000502:physiology; D007238:Infarction / Q000378:metabolism* / Q000473:pathology; D007668:Kidney / Q000098:blood supply* / Q000378:metabolism* / Q000473:pathology; D007685:Kidney Tubules, Collecting / Q000098:blood supply / Q000378:metabolism / Q000473:pathology; D008562:Membrane Glycoproteins / Q000378:metabolism*; D009399:Nephrons / Q000098:blood supply / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley
D027682:Cation Transport Proteins; D008562:Membrane Glycoproteins; C508142:Rh type B glycoprotein, rat; C508143:Rh type C glycoprotein, rat; D000641:Ammonia