In intestinal epithelial cells cytosolic Ca2+ leads to the opening of basolateral K+ -channels, increasing the driving force for chloride secretion. It is not clear yet, whether it also directly opens Cl-- channels. This was examined in an Ussing chamber study with porcine colon. Tissues were bathed in modified Krebs-Henseleit (KH)-buffer or in a K+ -rich buffer to depolarise the basolateral membrane. Some tissues were preincubated with NPPB to block CFTR channels or DIDS to block alternative Cl--channels. Stimulation of Cl--secretion was achieved by carbachol (Ca2+ - release) and forskolin (increase in cAMP). Tissues which had not been preincubated were treated with NPPB after forskolin. Blocking alternative Cl--secretion pathways did not change the extent of Cl--secretion. CFTR inhibition decreased basal Isc , strongly diminished Ca2+ -induced and abolished cAMP-induced Cl--secretion. In K+ -rich buffer basal Isc were lower than in KH- buffer. If basolateral K+ -channels could not increase the driving force for chloride secretion and CFTR channels were blocked, carbachol produced a negative Isc , which may be explained by a remaining K+ -secretion. Without inhibition of CFTR, Isc remained unchanged after carbachol, probably because K+ - and Cl--secretion masked each other. These results give no evidence of Ca2+ -activated chloride channels in the porcine colon.