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Am J Physiol Renal Physiol 283: F1011-F1019, 2002; doi:10.1152/ajprenal.00106.2002
0363-6127/02 $5.00
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Vol. 283, Issue 5, F1011-F1019, November 2002

Regulation of expression of the SN1 transporter during renal adaptation to chronic metabolic acidosis in rats

Anne M. Karinch, Cheng-Mao Lin, Christopher L. Wolfgang, Ming Pan, and Wiley W. Souba

Department of Surgery, Milton S. Hershey Medical Center, The Pennsylvania State University College of Medicine, Hershey, PA 17033

During chronic metabolic acidosis, renal glutamine utilization increases markedly. We studied the expression of the system N1 (SN1) amino acid transporter in the kidney during chronic ammonium chloride acidosis in rats. Acidosis caused a 10-fold increase in whole kidney SN1 mRNA level and a 100-fold increase in the cortex. Acidosis increased Na+-dependent glutamine uptake into basolateral and brush-border membrane vesicles (BLMV and BBMV, respectively) isolated from rat cortex (BLMV, 219 ± 66 control vs. 651 ± 180 pmol · mg-1 · min-1 acidosis; BBMV, 1,112 ± 189 control vs. 1,652 ± 148 pmol · mg-1 · min-1 acidosis, both P < 0.05). Na+-independent uptake was unchanged by acidosis in BLMV and BBMV. The acidosis-induced increase in Na+-dependent glutamine uptake was eliminated by histidine, confirming transport by system N. SN1 protein was detected only in BLMV and BBMV from acidotic rats. After recovery from acidosis, SN1 mRNA and protein and Na+-dependent glutamine uptake activity rapidly returned to control levels. These data provide evidence that regulation of expression of the SN1 amino acid transporter is part of the renal homeostatic response to acid-base imbalance.

renal acid-base homeostasis; basolateral membrane vesicle transport; brush-border membrane vesicle transport; ammonium chloride acidosis; system N1


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