Effects of pentylenetetrazol on ion transport in the isolated toad bladder

The effect of pentylenetetrazol (PTZ) on ion transport in the isolated toad bladder was investigated. 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 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 K+-Ringer's solution (118.5 mM) bathed the serosal surface, ADH caused an incrase in SCC, whereas the resonse to PTZ was abolished. In addition, a maximally effective dose of amphotericin B blocked the response to ADH but not that of PTZ. The unidirectional fluxes of 22Na nad 36CI were not changed following PTZ treatment; however, a percentage increase was observed in the muscosal to serosal 42K flux that matched the percentage increase in SCC. The stimulation of SCC evoked by PTZ is presumed to be relted to a decrease in membrane resistance accompanied by an efflux of K+ across the serosal embrane of the bladder. A specific PTZ-antaonist, trimethadione, inhibited the SCC increae caused by PTZ, Finally, the changes in SCC produced by a series of PTX structural analogues correlated closely with their convulsant potencies in mice. These results indicate the suitability of the toad bladder as a model system for studying the effects of a convulsant and anticonvulsant on membrane processes.