Abstract

Recent results from this laboratory have shown that in the absence of mucosal Na+ and exogenous CO2, H+ excretion is reduced in the toad urinary bladder. This study was done to determine if H+ excretion is linked to Na+ reabsorption in the toad bladder. Na+ transport was inhibited by ouabain or by substitution of the sodium with choline chloride. Both of these agents produced an inhibition of H+ excretion. However, when dinitrophenol was added to stimulated CO2 production by the tissue, H+ excretion returned to control levels even though Na+ transport was still inhibited. Vasorressin, which stimulates Na+ transport in toad urinary bladder, had no effect on H+ excretion. In addition, simultaneous energies of activation were detemined for H+ excretion and Na+ reabsorption in the toad bladder. The activation energies for the two processes were significantly different. These results suggest that Na+ and H+ are not coupled in an exchange mechanism at the mucosal surface of the cell. H+ excretion, however, does appear to be limited by the endogenous CO2 production of the bladder in the absence of exogenous CO2.

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