Acetylcholine‐evoked potassium release in the mouse pancreas.

Mouse pancreatic segments were superfused with physiological saline solutions and the K+ concentration in the effluent was measured by flame photometry. Acetylcholine (ACh) evoked a dose‐dependent and transient increase in the K+ concentration in the effluent (K+ release). The removal of calcium (Ca2+) from the superfusing solution and addition of 10(‐4) M‐EGTA (ethyleneglycol‐bis‐(beta‐amino‐ethylether)N,N'‐tetraacetic acid) caused a significant reduction in the ACh‐elicited K+ outflow. Pre‐treatment of pancreatic segments with the 'loop diuretics' (furosemide, piretanide and bumetanide; all 10(‐4) M) resulted in uptake of K+ into the tissue segments. The diuretics also caused a marked reduction in the ACh‐induced K+ release. Replacement of chloride (Cl‐) in the physiological salt solution by nitrate (NO3‐), sulphate (SO42‐) or iodide (I‐) caused K+ uptake and a significant reduction in the ACh‐evoked K+ release. However, when Cl‐ was replaced by bromide (Br‐) the response to ACh was virtually unaffected. When sodium (Na+) was replaced by lithium (Li+) ACh did not evoke K+ release but instead K+ uptake was observed. However, when Tris+ was substituted for Na+ ACh evoked a very small K+ release. Pre‐treatment of pancreatic segments with 10(‐3) M‐ouabain resulted in a marked sustained K+ release. In the continuing presence of ouabain ACh induced a further increase in K+ outflow. Pre‐treatment of the preparation with 10 mM‐tetraethyl‐ammonium (TEA) caused a small transient increase in K+ efflux, but TEA had virtually no effect on the secretagogue‐evoked changes in effluent K+ concentration. The results suggest the presence of a diuretic‐sensitive Na+‐K+‐Cl‐ co‐transport system in the mouse pancreatic acinar membrane.