Passive transepithelial absorption of thyrotropin-releasing hormone (TRH) via a paracellular route in cultured intestinal and renal epithelial cell lines.

摘要: Transport studies using intestinal brush-border membrane vesicles isolated from rats and rabbits have failed to demonstrate proton- or Na+-dependent carrier-mediated transport of thyrotropin-releasing hormone (TRH), despite a pharmacologically relevant oral bioavailability. To examine the hypothesis that reported levels bioavailability reflect predominately paracellular rather than transcellular route for transepithelial TRH, we studied TRH in cultured epithelial cell types (Caco-2 T84) renal (MDCK I, MDCK II, LLC-PK1 origin, whose pathways span range permeability values observed natural epithelia. across monolayers Caco-2 cells was similar flux mannitol (1–4% per 4 hr), unlike other putative substrates di-/tripeptide carrier, apical-to-basolateral not increased by presence an acidic pH apical chamber. did show saturation, being uneffected 20 mM cold TRH. In each type were positively correlated with conductance layers, consistent passive mechanism absorption. This evidence suggests that, providing peptide is resistant luminal hydrolysis, small but significant amounts absorption may be achieved route.