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. Changes in ammonium excretion with acid/base perturbations are dependent on changes in medullary ammonium accumulation mediated by active NH 4  +  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 + (NH 4  + )/2Cl - -cotransporter (BSC-1), the apical Na + /H + -exchanger (NHE3), and the Na + /K + -ATPase α1-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 NH 4 Cl (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 NaHCO 3  (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 NaHCO 3  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) NaHCO 3  or NaCl. It is concluded that outer medullary BSC-1 and Na + /K + -ATPase α1-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 NH 4 Cl loading.

Regulation of Thick Ascending Limb Ion Transporter Abundance in Response to Altered Acid/Base Intake