Acetylcholine‐evoked potassium release in the mouse pancreas.

Abstract

SUMMARY1. Mouse pancreatic segments were superfused with physiological saline solutions and the K+ concentration in the effluent was measured by flame photometry.2. Acetycholine (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-(f-aminoethylether)N,N'-tetraacetic acid) caused a significant reduction in the ACh-elicited K+ outflow.3. 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.4. Replacement ofchloride (Cl-) in the physiological salt solution by nitrate (NO3), sulphate (SO42-) or iodide (-) caused K+ uptake and a significant reduction in the ACh-evoked K+ release. However, when Cl-was replaced by bromide (Br-) the response to AChf was virtually unaffected.5. 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.6. 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-tetraethylammonium (TEA) caused a small transient increase in K+ efflux, but TEA had virtually no effect on the secretagogue-evoked changes in effluent K+ concentration.7. The results suggest the presence of a diuretic-sensitive Na+-K+Cl-co-transport system in the mouse pancreatic acinar membrane.

Acetylcholine‐evoked potassium transport in the isolated guinea‐pig pancreas

“…In contrast to previous studies in either mice (Petersen & Singh, 1985;Exley et al 1986) Effect of Cl -removal on ACh-elicited K + release The effect of Cl-removal on the ACh-evoked K+ release was investigated in a number of experiments. Cl-in the superfusing medium was replaced by either NO3-or Br-.…”

“…The effluent from the tissue chamber was passed directly to an on-line flame photometer and the potassium concentration ([K+]O) measured following the method of Petersen & Singh (1985 Figure the peak of the response after application of 10-6 M ACh. In contrast to previous studies in either mice (Petersen & Singh, 1985;Exley et al 1986) Effect of Cl -removal on ACh-elicited K + release The effect of Cl-removal on the ACh-evoked K+ release was investigated in a number of experiments.…”

“…In mouse pancreatic acinar cells, receptor activation leads to the opening of calcium-activated voltage-insensitive non-selective cation channels on the basolateral membrane (Maruyama & Petersen, 1982 a, b;Maruyama, Gallacher & Petersen, 1983). There is also evidence for the presence of a diuretic-sensitive Na+-K+-2Cl-cotransporter in mouse pancreatic acinar cells (Singh, 1984;Petersen & Singh, 1985) but it appears to move ions from the intracellular to the extracellular compartment, in the opposite direction to the same cotransporter in salivary acini (Exley, Fuller & Gallacher, 1986;Petersen & Maruyama, 1989). This means that if the cotransporter plays a role in secretion, then it must be located on the luminal membrane (Petersen & Singh, 1985).…”

“…There is also evidence for the presence of a diuretic-sensitive Na+-K+-2Cl-cotransporter in mouse pancreatic acinar cells (Singh, 1984;Petersen & Singh, 1985) but it appears to move ions from the intracellular to the extracellular compartment, in the opposite direction to the same cotransporter in salivary acini (Exley, Fuller & Gallacher, 1986;Petersen & Maruyama, 1989). This means that if the cotransporter plays a role in secretion, then it must be located on the luminal membrane (Petersen & Singh, 1985). In rats, it was suggested that chloride accumulation across the basolateral membrane could best be explained by a combination of Na+-H+ and Cl--HCO3-exchange rather than by a Na+-K+-2CI-cotransporter (Hellmessen, Christian, Fasold & Schulz, 1985;Seow, Lingard & Young, 1986).…”

“…Released K+ is then reaccumulated into the acinar cell by the Na+-K+ pump and also by a diuretic-sensitive Na+-K+-2Cl-cotransporter localized on the basolateral membrane (Petersen & Singh, 1985;Suzuki & Petersen, 1988).…”