[Architectural ultrastructure of the urinary bladder epithelium. II. Changes in the urine-blood barrier in the contracted and distended state in the normal and inflammatory bladder].

The urinary bladder epithelium in mammals, including humans, has a low permeability to ions and small molecules such as sodium, urea and water. Two structures, asymmetrical luminal plasma membrane and tight junction between superficial cells, have been said responsible for the urine-blood barrier. The permeability of junctional complex between superficial cells to lanthanum was observed in rat urinary bladder epithelium by transmission electron microscopy (TEM). In the normal bladder epithelium, confirmed by bacteriological examination, most junctions between superficial cells are the tight junctions and 1 to 9% of the junctions are leaky. The lanthanum, known to penetrate the leaky junctions, is demonstrated in the intercellular space between intermediate and basal cells. This suggests that desmosomes between these cells have no barrier function. In the experimentally inflammatory bladder epithelium all junctions are tight and no leaky junction is found between superficial cells. In contrast, if the superficial cells were stripped off in the inflammatory change, the lanthanum penetrates the junction between denuded intermediate cells. In the normal bladder epithelium the structural junctions between superficial cells have no changes during contraction and distension. Thus this suggests that the permeability to lanthanum does not change during contraction and distension.