Basal Fluxes Research Articles

Antisecretory effects of berberine in rat ileum.

The in vitro antisecretory effects of the alkaloid berberine (1.0 mM) on intestinal ion secretion and mucosal adenylate cyclase and Na-K-ATPase activities were studied in the rat ileum. Mucosal berberine did not alter the individual basal net ion fluxes and basal adenylate cyclase activity but decreased short-circuit current (Isc) and increased the net absorption of chloride plus bicarbonate. In the cholera toxin-treated tissue, mucosal berberine stimulated absorption of Na and Cl and inhibited the increased adenylate cyclase activity but did not change the specific Na-K-ATPase activity, whereas serosal berberine stimulated Na secretion and decreased Isc. Mucosal berberine also decreased Isc, increased Cl permeability, and reversed the ion secretion induced by dibutyryl cyclic AMP, the heat-stable enterotoxin of Escherichia coli, and methylprednisolone administration. The antisecretory effects of mucosal berberine may be explained by stimulation of a Na-Cl-coupled absorptive transport process. The mechanism of action of serosal berberine remains to be elucidated. However, it is clear that mucosal berberine affects intestinal ion transport by mechanisms different from stimulation of the Na pump and probably at a step distal to the production or degradation of cyclic AMP or cyclic GMP.

Transmembrane components of taurine flux across frog retinal pigment epithelium.

In previous work from this laboratory, a net transepithelial flux of the amino acid taurine was measured across the in vitro frog retinal pigment epithelium. This flux was from retina to choroid and could be modulated by small (0.5 mM) changes in K+ concentration, by changes in taurine concentration, and by ouabain. In the present experiments we measured the unidirectional transmembrane fluxes across each of the two cell membranes, the apical membrane (facing the neural retina) and the basal membrane (facing the choroid) of the retinal pigment epithelium. In modified Ringer's solution containing 2mM taurine + 2mM K+, we found that the apparent outward permeability of the basal membrane, corrected for its actual area, was 26 times that of the apical membrane. As expected from the direction of net flux, the inward apical and outward basal fluxes dominated the transmembrane fluxes. When the apical Na+:K+ pump was inhibited, the ratio of the apparent permeability of the basal membrane relative to the apical decreased from 26 to 4.4. The data are consistent with the previous suggestion of Na+:taurine co-transport into the retinal pigment epithelium across the apical membrane. The basal membrane response to ouabain and reduced K+ concentration suggests that a K+-dependent mechanism is responsible, at least in part, for the inward basal taurine flux.