ACETYLCHOLINE‐EVOKED POTASSIUM AND SODIUM TRANSPORT IN RAT LACRIMAL SEGMENTS: EVIDENCE FOR A SODIUM‐CHLORIDE CO‐TRANSPORT SYSTEM

1988 
An investigation was made of the effects of acetylcholine (ACh) on transmembrane movements of potassium (K+) and sodium (Na+) in isolated segments of rat lacrimal glands. ACh elicited dose-dependent and transient increases in K+ concentration in the effluent (K+ release). The ACh-induced K+ outflow was unaffected by either pre-treatment of lacrimal segments with loop diuretics (frusemide, piretanide and bumetanide, all 10−4 M) or replacement of chloride (Cl−) in the physiological salt solution with nitrate (NO3−). In contrast, ACh caused a significant (P 〈 0·001) reduction in Na+ concentration in the effluent (Na+ uptake). The ACh-evoked Na+ uptake was sensitive to loop diuretics and Cl− removal. Pre-treatment of tissue with ouabain (10−3 M) resulted in a marked sustained K+ release. ACh produced a further increase in K+ efflux in the continuing presence of ouabain. Incubation of the tissue with 10 mM-tetraethylammonium (TEA) resulted in an uptake of K+. The results suggest the presence of a diuretic-sensitive Na+-Cl− co-transport system in lacrimal acinar cell membranes.
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