Acetylcholine-evoked potassium and sodium transport in rat lacrimal segments: evidence for a sodium-chloride co-transport system.

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 less than 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 result suggest the presence of a diuretic-sensitive Na+-Cl- co-transport system in lacrimal acinar cell membranes.