title: Deposition of BaSO4 in the tight junctions of amphibian epithelia causes their opening; apical Ca2+ reverses this effect.
abstract: Selective deposition of BaSO4 in the tight junctions (TJs) of frog skins led to profound and reversible functional alterations of these structures, as revealed by changes of tissue conductance (G), clamping current (I), and fluxes of extracellular markers (sulfate (JSO4) and sucrose (JSUC)). Experiments were performed with nominally Ca(2+)-free simple salt solutions on the apical side (usually KCl) and Na2SO4-Ringer on the inner side of skins. The deposition of BaSO4 in the TJs was obtained by diffusion and/or migration through the paracellular path of Ba2+ from the apical solution and SO4(2-) from the inner solution. A brief presence (2 to 6 min) of apical Ba2+ (Ba2+ pulse) is followed (i.e., when Ba2+ is removed from the apical fluid) by a large increase of G, I, JSO4 and JSUC, above pre-Ba2+ levels. These attain a steady state within 15 to 30 min (overshoot phase), characterizing a conspicuous increase of the paracellular permeability. During the overshoot phase, a second Ba2+ pulse blocks the paracellular route while apical Ba2+ is present, leading to a new and larger overshoot when the Ba2+ pulse is terminated. Addition of apical Ca2+ triggers the resealing of the TJs, resulting in a full recovery of G, I, JSO4 and JSUC. This Ca(2+)-induced recovery persists when apical Ca2+ is removed. The presence of a normal Ca2+ concentration in the inner bathing Ringer does not induce the recovery process. Tissues remain viable after being submitted to the Ba2+ treatment and the subsequent overshoot. Experiments performed in the urinary bladder of Rana catesbeiana and skins and urinary bladders of Bufo marinus indicate that Ba2+ effect can also be elicited in these tissues. The above results seem to report general properties of the TJs. Incidentally, they warn about the use of Ba2+ as an ion channel blocker in epithelial membranes in association with SO4(2-)-containing solutions on the contralateral side.
authors.affiliation: Departamento de Ciências Fisiológicas, Universidade do Rio Grande, RS, Brasil.
authors.forename: J A
authors.initials: JA
authors.lastname: Castro
authors.forename: A
authors.initials: A
authors.lastname: Sesso
authors.forename: F
authors.initials: F
authors.lastname: Lacaz-Vieira
mesh_terms: D000818:Animals; D001464:Barium / Q000378:metabolism; D001466:Barium Sulfate / Q000378:metabolism*; D002024:Bufo marinus; D002118:Calcium / Q000378:metabolism*; D002463:Cell Membrane Permeability; D004553:Electric Conductivity; D004848:Epithelium / Q000378:metabolism; D007365:Intercellular Junctions / Q000378:metabolism* / Q000648:ultrastructure; D007473:Ion Channels / Q000378:metabolism; D008854:Microscopy, Electron; D011188:Potassium / Q000378:metabolism; D011892:Rana catesbeiana; D012867:Skin / Q000378:metabolism; D012964:Sodium / Q000378:metabolism; D012996:Solutions; D014508:Urea / Q000494:pharmacology
chemical_list: D007473:Ion Channels; D012996:Solutions; D001464:Barium; D001466:Barium Sulfate; D014508:Urea; D012964:Sodium; D011188:Potassium; D002118:Calcium