An examination of functional linkage between K efflux and 36Cl efflux in rat submandibular salivary gland acini in vitro.

Suspensions of dispersed acini isolated by enzymatic (collagenase) digestion were used to investigate possible interactions between transmembrane K and Cl movements. The isotopic tracer 36Cl monitored uptake and efflux of Cl under conditions where K efflux was either stimulated or inhibited. Uptake (accumulation) of 36Cl in the absence of experimental manipulation was time-dependent, resulting in a steady-state isotope content of 8.9 +/- 0.2 nmol/mg protein after 3-5 min of incubation. This content was reduced 28 per cent by the K-ionophore, valinomycin (10 microM), which also caused a net efflux of 36Cl (28 per cent) from tracer-preloaded acini. Valinomycin also released 38 per cent of the cellular K content and caused efflux of 86Rb from acini preloaded with this tracer. The efflux of 36Cl induced by 1 microM acetylcholine (23 per cent) was blocked by the K-channel blocker, quinidine (1 mM), and incompletely by apamin (1 mM). Efflux of 36Cl was also blocked by the chloride-channel blocker, 3,5-dichlorophenyl-2-amine-carboxylic acid. Thus, induction of K release (efflux) in these acini is balanced by a parallel efflux of Cl, and blockade of K release inhibits acetylcholine-induced 36Cl efflux, which suggests a functional linkage between these two events. According to current opinion, these ion movements occur, respectively, in the basolateral (K) and apical (Cl) cell membranes, so any linkage implies that the apical Cl conductance can be regulated, at least in part, by changes in membrane potential which are secondary to secretagogue-induced changes in K conductance.(ABSTRACT TRUNCATED AT 250 WORDS)