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

In this study, K+ concentration was measured in effluent samples from superfused guinea‐pig pancreatic pieces in control conditions and during stimulation with ACh, employing the technique of flame photometry. ACh (10(‐7)‐10(‐5) M) evoked a dose‐dependent and sustained increase in K+ concentration in the effluent (K+ release). The removal of Ca2+ from the superfusing medium and the addition of 10(‐4) M EGTA caused a significant (P < 0.05) reduction in the ACh‐evoked K+ efflux. Replacement of extracellular Cl‐ in the superfusing physiological salt solution with NO3‐ abolished the ACh‐induced K+ efflux. In contrast, when Cl‐ was replaced with Br‐, ACh still evoked marked K+ release. Pretreatment of pancreatic segments with the loop diuretic furosemide (10(‐4) M) resulted in an inhibition of K+ efflux elicited by ACh. Stimulation of pancreatic segments with the Na(+)‐K(+)‐ATPase inhibitor ouabain (10(‐3) M) caused a large efflux of K+. In the continuous presence of ouabain, ACh application elicited no further change in the K+ release. The results indicate that ACh‐evoked K+ release from guinea‐pig pancreatic segments is sensitive to ouabain, Cl‐, furosemide and extracellular Ca2+ and that only the basal efflux is augmented by ouabain. The findings provide further evidence that a diuretic‐sensitive coupled Na(+)‐K(+)‐Cl‐ cotransport system operates in the guinea‐pig pancreas, as it does in other similar transporting epithelia, to bring about K+ mobilization.