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*
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and
Blood Institute, National Institutes of Health, Bethesda, Maryland
Department of Biological Sciences, George Washington University,
Washington, DC
Correspondence to Dr. Mark A. Knepper, National Institutes of Health, Building 10, Room 6N260, 10 Center Drive MSC 1603, Bethesda, MD 20892-1603. Phone: 301-496-3064; Fax: 301-402-1443; E-mail: knep{at}helix.nih.gov
Abstract. Changes in ammonium excretion with acid/base
perturbations are dependent on changes in medullary ammonium accumulation
mediated by active NH4+ absorption by the medullary
thick ascending limb. To investigate whether alterations in the abundance of
medullary thick ascending limb ion transporters, namely the apical
Na+/K+(NH4+)/2Cl--cotransporter
(BSC-1), the apical Na+/H+-exchanger (NHE3), and the
Na+/K+-ATPase 
1-subunit, may be responsible in
part for altered medullary ammonium accumulation, semiquantitative
immunoblotting studies were performed using homogenates from the inner stripe
of the rat renal outer medulla. After 7 d of NH4Cl (7.2 mmol/220 g
body wt per d) loading (associated with increased medullary ammonium
accumulation), neither BSC-1 nor Na+/K+-ATPase protein
expression was altered, but NHE3 protein abundance was significantly
increased. On the other hand, both BSC-1 and
Na+/K+-ATPase protein abundance was increased
significantly in rats fed NaHCO3 (7.2 mmol/220 g body wt per d) for
7 d. Rats fed a high-NaCl diet (7.7 mEq Na+/220 g body wt per d)
for 5 d also showed marked increases in both BSC-1 and
Na+/K+-ATPase expression. The expression level of NHE3
protein did not change with either NaHCO3 or high NaCl intake. None
of these three transporters showed a significant difference in abundance
between the groups fed equimolar (7.2 mmol/220 g body wt per d for 7 d)
NaHCO3 or NaCl. It is concluded that outer medullary BSC-1 and
Na+/K+-ATPase 1-subunit protein abundance is
increased by chronic Na+ loading but not by acid/base perturbations
and that outer medullary NHE3 protein abundance is increased by chronic
NH4Cl loading.
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T.-H. Kwon, J. Frokiar, J. S. Han, M. A. Knepper, and S. Nielsen Decreased abundance of major Na+ transporters in kidneys of rats with ischemia-induced acute renal failure Am J Physiol Renal Physiol, June 1, 2000; 278(6): F925 - F939. [Abstract] [Full Text] [PDF]
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W. Wang, T.-H. Kwon, C. Li, J. Frokiar, M. A. Knepper, and S. Nielsen Reduced expression of Na-K-2Cl cotransporter in medullary TAL in vitamin D-induced hypercalcemia in rats Am J Physiol Renal Physiol, January 1, 2002; 282(1): F34 - F44. [Abstract] [Full Text] [PDF]
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T.-H. Kwon, C. Fulton, W. Wang, I. Kurtz, J. Frokiar, C. Aalkjar, and S. Nielsen Chronic metabolic acidosis upregulates rat kidney Na-HCO3- cotransporters NBCn1 and NBC3 but not NBC1 Am J Physiol Renal Physiol, February 1, 2002; 282(2): F341 - F351. [Abstract] [Full Text] [PDF]
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