Urinary acidification in turtle bladder is due to a reversible proton-translocating ATPase.

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Abstract
Adverse proton electrochemical gradients (.DELTA.~.mu.H) applied across the turtle urinary bladder decrease active H+ transport in this epithelium. A .DELTA.~.mu.H of 180 mV abolishes both transport and its tightly coupled metabolic reaction. Larger gradients should, in theory, reverse the direction of H+ transport and the metabolic reaction leading to synthesis of ATP if the pump is an ATPase, or cause an increase in the oxidized state of a redox pair if it is a redox pump. ATP levels were measured in epithelial cells that were poisoned to inhibit cellular mechanisms of ATP synthesis. At .DELTA.~.mu.H of 120 mV or less no ATP synthesis was found. At .DELTA.~.mu.H of greater than 120 mV there was a linear increase in ATP synthesis. Dinitrophenol, a H+ carrier, prevented synthesis at .DELTA.~.mu.H of 310 mV. Dicyclohexylcarbodiimide, an inhibitor of H+ transport that works at the cell surface, prevented ATP synthesis at .DELTA.~.mu.H of 310 mV. A reversible proton-translocating ATPase in the mucosal border of the bladder is the H+ pump responsible for urinary acidification.