The efflux of both chloride and potassium ions are important for secretion in equine sweat gland epithelial cells. Purinergic agonists have been shown to increase apical chloride efflux in these cells (Jenkinson et al. 2006). The mechanisms involved in purinergic-induced chloride secretion are not fully known. The efflux of chloride ions is maintained by a hyperpolarising efflux of potassium ions from the cells. Calcium-activated potassium channels (BK channels) have been identified in these cells (Huang et al. 1999), however, it is not known if these channels support chloride efflux in equine cells. The study investigated the involvement of BK channels in supporting the chloride efflux elicited by purinergic agonists. Equine sweat gland epithelial cells were grown on permeable supports and mounted in Ussing chambers for electrophysiology. Paxilline, a potent BK channel blocker, was applied to the cells apically, basolaterally, or both simultaneously and the responses to apically applied ATP and UTP were monitored under open circuit conditions. Statistical analyses were carried out using Student’s t-test, where P<0.01 was considered significant. Results are presented as mean ± SEM. Blocking of BK channels, either apically or basolaterally only, had no effect on chloride efflux brought about by stimulation with ATP or UTP. When BK channels were blocked apically and basolaterally simultaneously, chloride efflux in response to ATP was not affected, however, there was a significant increase in chloride efflux in response to UTP (see figures 1 & 2). These results indicate that the mechanisms of chloride efflux differ in response to ATP and UTP in equine sweat gland epithelial cells. BK channels do not appear to have any involvement in ATP-induced chloride efflux in these cells, whereas the UTP results suggest that BK channels have an inhibitory effect on secretion, as blocking these channels significantly increased chloride efflux from these cells.