Abstract

The effect of pentylenetetrazol (PTZ) on various bioelectric parameters and on ²²Na, ³⁶Cl and ⁴²K fluxes was investigated in the isolated toad bladder. PTZ produced an increase in short-circuit current (SCC) when placed in the serosal-side bathing medium but no response when placed in the mucosal-side bathing medium. A comparison was made between PTZ and vasopressin (ADH). PTZ caused an increase in SCC when K⁺-free Ringer's solution bathed the serosal surface of the bladder, whereas the normal increase in SCC produced by ADH was abolished. In contrast, when high K⁺-Ringer's solutioun (118.5 mM) bathed the serosal surface, ADH caused an increase in SCC. whereas the response to PTZ was abolished. In addition, a maximally effective dose of amphotericin B blocked the response to ADH but not that to PTZ. The unidirectional fluxes of ²²Na and ³⁶Cl were not changed after PTZ treatment: however, a percent increase was observed in the mucosal to serosal ⁴²K flux that matched the percent increase in SCC. The stimulation of SCC evoked by PTZ may be related to a decrease in membrane resistance accompanied by an efflux of K⁺ across the serosal membrane of the bladder. A specific PTZ antagonist, trimethadione, inhibited the SCC increase caused by PTZ. Finally, a series of PTZ structural analogs produced changes in SCC which suggested that the cellular action of this group of convulsants in toad bladder may be similar to their action in the central nervous system.