In the present study, we characterized the effects of the calcium (Ca 2+) channel activator BAY K 8644 on sodium (Na +) absorption and transepithelial potential difference (Pd) in the rabbit gall-bladder. In gall-bladders mounted in an Ussing chamber it was observed that serosal BAY K 8644 (10 -s M) inhibited Na + absorption in the presence, but not in the absence of serosal Ca 2+. Serosal nifedipine (a Ca 2+ channel antagonist) at 10 -5 M did not reverse the Na + transport inhibition caused by BAY K 8644. Another effect of serosal BAY K 8644 (10 -5 M) was to induce oscillations in Pd. These Pd-oscillations had a frequency of about one per minute and an amplitude of 20-40 ~tV. The appearance of Pd-oscillations was dependent on the presence of Ca 2 + in the serosal medium. The oscillations were abolished by 1 -3 x 10-5 M serosal nifedipine and by bilateral application of 3 mM barium (Ba 2 +) (a K + channel blocker). In a sac preparation of the rabbit gall-bladder, spontaneous cyclic contractions of smooth muscle cells in the gall-bladder wall were observed as oscillations in the transmural pressure. These spontaneous contractions were not accompanied by oscillations in Pd. Serosal BAY K 8644 (10 -5 M) evoked oscillations in Pd in half of the sac preparations, but in each gall-bladder the frequencies of Pdoscillations and pressure oscillations were different. Serosal nifedipine (2 x 10-5 M) abolished both types of oscillation. The results show that the BAY K 8644-induced Na + transport inhibition and initiation of Pd-oscillations can be ascribed to specific epithelial Ca 2 +-dependent effects of BAY K 8644. We postulate that the Pd-oscillations involve Ca 2 +activated, Ba 2 +-sensitive K + channels in both the luminal and the basolateral cell membrane.