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Rat urinary bladder epithelial cells exhibited a membrane potential of about -22 (apical) and -24 (basal) mV in normal Krebs solution. Blockade of Na+ entry through the apical membrane by Na+ depletion of administration of amiloride, or inactivation of the Na pump in the basal membrane by ouabain resulted in marked hyperpolarization of the epithelial cells. N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN), a specific carcinogen, and saccharin, a potent enhancer of carcinogenesis, inhibited development of the Na+ channel and/or Na pump on the bladder epithelium. This physiology may contribute to the abnormal intracellular environment leading to bladder carcinoma.
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