Urinary Ca2+ and the regulation of K+ secretion in toad bladder by neurohypophyseal hormones.

Abstract

We measured net K+ fluxes in the isolated toad urinary bladder to determine whether neurohypophyseal hormones control K+ secretion in this tissue. To determine if the pathway involved in K+ secretion is similar to a Ca(2+)-blockable alkali cation channel in the apical membrane of toad bladder, previously described in electrophysiological studies, we measured K+ fluxes in either the presence or absence of Ca2+ in the mucosal bathing solution. Oxytocin enhanced K+ secretion in both cases; however, the enhancement was markedly greater in the absence of mucosal Ca2+. In other experiments the transepithelial voltage was held constant at a value of 120 mV (mucosa negative) to find whether hyperpolarization would enhance K+ secretion to the levels seen in Ca(2+)-free solutions. The response to oxytocin was markedly greater in the absence of mucosal Ca2+ even when the transepithelial voltage was continuously hyperpolarized. These observations suggest that the properties of the activated pathway are akin to those of the previously described Ca(2+)-blockable alkali cation channel. We also found that toad bladder urine often contained extremely low levels of Ca2+; therefore neurohypophyseal hormonal control of K+ transport across the bladder may play an important role in amphibian K+ balance.