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Am J Physiol Renal Physiol (September 21, 2001). doi:10.1152/ajprenal.00104.2001
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Articles in PresS, published online ahead of print September 21, 2001
Am J Physiol Renal Physiol, 10.1152/ajprenal.00104.2001
Submitted on March 26, 2001
Accepted on September 14, 2001

Chronic metabolic acidosis upregulates rat kidney Na,HCO3 cotransporters NBCn1 and NBC3 but not NBC1

Tae-Hwan Kwon1, Christiaan Fulton2, Weidong Wang2, Ira Kurtz3, Jorgen Frokiaer2, Christian Aalkjaer2, and Soren Nielsen2*

1 The Water and Salt Research Center, University of Aarhus, Aarhus, Denmark; Department of Physiology, Dongguk University, Kyungju, Korea, Republic of
2 The Water and Salt Research Center, University of Aarhus, Aarhus, Denmark
3 Division of Nephrology, UCLA School of Medicine, Los Angeles, CA, USA

* To whom correspondence should be addressed. E-mail: sn{at}ana.au.dk.

Several members of the Na,HCO3 cotransporter (NBC) family have recently been identified, functionally and partly characterized including rkNBC1, NBCn1, and NBC3. Regulation of these NBCs may play a role in the maintenance of intracellular pH and in renal regulating acid/base balance. However it is unknown whether the expressions of these NBCs are regulated in response to changes in acid/base status. We therefore tested whether chronic metabolic acidosis (CMA) affects the abundance of these in kidneys using two conventional protocols. Protocol 1: Rats were treated with NH4Cl in drinking water (12± 1 mmol/rat/day) for 2 wks with free access to water (n=8). Semiquantitative immunoblotting demonstrated that whole kidney abundance of NBCn1 and NBC3 in rats with CMA was dramatically increased to 995 ± 87% and 224 ± 35% of control levels (P<0.05), whereas whole kidney rkNBC1 was unchanged (88 ± 14%). Protocol 2: Rats were given NH4Cl in the food (10 ± 1 mmol/rat/day) for 7 days with fixed daily water intake (n=6). Consistent with protocol 1, whole kidney abundances of NBCn1 (262± 42%) and NBC3 (160 ± 31%) were significantly increased compared to controls (n=6), whereas whole kidney rkNBC1 was unchanged (84 ± 17%). In both protocols immunocytochemistry confirmed upregulation of NBCn1 and NBC3 with no change in the segmental distribution along the nephron. Consistent with the increase in NBCn1, measurements of pH transients in mTAL cells in kidney slices revealed 2-3 fold increases in DIDS sensitive, Na+-dependent-HCO3? uptake in rats with CMA. In conclusion, CMA is associated with a marked increase in the abundance of NBCn1 in the mTAL and NBC3 in the IC whereas the abundance of NBC1 in the proximal tubule was not altered. The increased abundance of NBCn1 may play a role in reabsorbing NH4+ in the mTAL and the increased NBC3 in reabsorbing HCO3-.




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