Effects of acetylcholine and caerulein on 86Rb+ efflux in the mouse pancreas. Evidence for a sodium-potassium-chloride cotransport system.

The effects of acetylcholine and the cholecystokinin-like peptide, caerulein on the fractional efflux of 86Rb+ from preloaded isolated segments of mouse pancreas were studied. Both secretagogues evoked a marked transient increase in 86Rb+ efflux. The removal of Ca2+ from the superfusing medium and addition of 10(-4) M EGTA, markedly reduced, but did not abolish the responses to either acetylcholine or caerulein. Furosemide (10(-5)-10(-3) M) or piretanide (10(-4) M) reduced the basal efflux and inhibited the secretagogue-elicited responses. Stimulus-induced 86Rb+ outflow was abolished when the Cl- component of the superfusing solution was replaced by either NO3-, SO42- or I- but not in case of replacement by Br-. When Na+ was replaced with either Li+ or choline+ both acetylcholine and caerulein failed to elicit any detectable increase in 86Rb+ outflow. However, when Tris+ was substituted for Na+, acetylcholine caused a moderate increase in 86Rb+ efflux which was abolished by either furosemide (10(-4) M) or chloride depletion (nitrate substitution). The removal of extracellular K+ or pretreatment with 10(-3) M ouabain had little effect on secretagogue-evoked 86Rb+ efflux. These results indicate the presence of a diuretic-sensitive Na+-K+-Cl- cotransport system in the mouse pancreatic acinar cell membrane.