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Kidney oxygen consumption, carbonic anhydrase, and proton secretion

Division of Nephrology-Hypertension, University of California, and Veterans Affairs San Diego Healthcare System, San Diego, California

Submitted 23 August 2005 ; accepted in final form 6 December 2005

Oxygen consumed by the kidney (Q_O2) is primarily obligated to sodium reabsorption (T_Na). The relationship of Q_O2 to T_Na (Q_O2/T_Na) may be altered by hormones and autacoids. To examine whether Q_O2/T_Na depends on the mechanism of sodium reabsorption, we first evaluated the effects on Q_O2 and Q_O2/T_Na of benzolamide (BNZ), a proximal diuretic that works by inhibiting membrane carbonic anhydrase. During BNZ infusion in anesthetized rats, Q_O2 increased by 50% despite a 25% decline in T_Na. However, BNZ failed to increase Q_O2/T_Na when given along with the adenosine A1 receptor blocker, DPCPX, which inhibits basolateral Na-bicarbonate cotransport (NBC1), or EIPA, which inhibits sodium-hydrogen exchange (NHE). Incubating freshly harvested rat proximal tubules with BNZ also caused Q_O2to increase by 62%, an effect that was prevented by blocking the apical NHE3 with S3226. Blocking NBC1 or NHE3 in the proximal tubule will have opposite effects on cell pH, but both maneuvers should reduce active chloride transport. In conclusion, inhibiting membrane carbonic anhydrase in the proximal tubule increases Q_O2 and reduces the energy efficiency of sodium reabsorption by the kidney. This is not purely due to shifting the burden of reabsorption to a more expensive site downstream from the proximal tubule. Instead, increased cost may be incurred within the proximal tubule as the result of increased active chloride transport.

NaCl reabsorption; transport efficiency; proximal tubule; benzolamide; adenosine; sodium-hydrogen exchange

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