Martinez J R, Barker S
Department of Child Health, University of Missouri School of Medicine, Columbia 65212.
Arch Oral Biol. 1987;32(11):843-7. doi: 10.1016/0003-9969(87)90012-4.
Dispersed acini were used to investigate the effects of prostaglandins (PG) on transmembrane Cl and K transport with the aid of radioactive tracers. Neither PGE1, PG2, PGF2 alpha, arachidonic acid or phosphatidic acid (all in 1 microM final concentrations) modified the time-dependent uptake of 36Cl. Steady-state isotope content reached 6-7 nmol/mg protein with or without these substances. PG did not alter the inhibitory effect of 1 mM furosemide on 36Cl uptake, and failed to induce a net efflux of 36Cl from tracer-preloaded cells or to modify the efflux of tracer induced by 1 microM acetylcholine. PG had no significant effect on K uptake, as measured with 86Rb, and did not modify the effect of 1 mM ouabain, which inhibited K uptake or accumulation by 60 per cent. PG did not induce K (86Rb) efflux from acini preloaded with tracer, and did not prevent or enhance the K efflux induced by acetylcholine. Thus PG do not influence the major ion-transport systems that may be involved in saliva secretion by acinar cells. Any inhibitory effects of PGE1 on salivary-fluid secretion in vivo are therefore likely to be the result of extra-acinar PG actions, and not of a direct effect on ion-transport mechanisms.