The ability of an epithelium to prevent permeation of noxious agents has not been well studied except in the gastrointestinal tract where exclusion of H+ has clinical significance. This article reviews the permeation routes across epithelia both as elucidated in the extensive electrophysiological work done in recent years and as demonstrated in morphological studies. We thus place concepts about gastrointestinal barrier function into the framework of transport physiology. Both the permeability and permselectivity of epithelial barriers are reviewed here. The effects of physical agents (pressure and electric current), polyvalent cations, organic compounds with both specific (channel blocking) and nonspecific (detergent) membrane properties, cyclic nucleotides, microfilament-active agents, and particularly H+ on both the barrier function (permeability and permselectivity) and transport function of epithelia are considered. Based on the available data, an important role for active Na+ transport in the maintenance of the epithelial barrier function can be postulated.
To assess Na-K-ATPase inhibiton and prostaglandin synthesis stimulation as the mechanism of the secretory (cathartic) action of phenolphthalein in the primate, we investigated water and electrolyte transport and Na-K-ATPase levels in monkey intestine. Both jejunum and colon were studied with in vivo perfusion and in vitro Ussing chamber techniques. Water, Na, and Cl absorption was inhibited or secretion was induced by phenolphthalein (10(-3) M) in the jejunum and colon when the drug was present in the mucosal bathing (perfusion) solution. Serosal addition of phenolphthalein (10(-4) or 10(-3) M) induced Na and anion absorption in the jejunum but not in the colon. Phenolphthalein inhibited Na-K-ATPase activity in the test tube, but assays of intestine previously perfused or bathed in the drug showed no inhibiton. Indomethacin, in doses sufficient to inhibit prostaglandin synthesis in the intestine, inhibited the secretion induced by phenolphthalein in the jejunum but not in the colon. These inconsistencies cast doubt on the role of Na-K-ATPase inhibition or the role of prostaglandin synthesis stimulation in the mechanism of action of phenolphthalein.
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