Inhibition of basolateral cAMP permeability in the toad urinary bladder.

1. The effect of sulphonylurea drugs on hydrosmotic flow across toad urinary bladder epithelium was re-evaluated in the present study. Glibenclamide, added to the basolateral medium, significantly enhanced the osmotic flow induced by low doses of antidiuretic hormone (ADH) or forskolin (FK), while it inhibited the effect of exogenous cyclic adenosine monophosphate (cAMP) or its non-hydrolysable bromo derivative, 8-Br-cAMP, added to the basolateral medium. These opposite effects of glibenclamide on the transepithelial osmotic flow can be explained by a reduction of cAMP permeability across the basolateral membrane of the epithelium. The decrease in cAMP permeability leads, according to the direction of the cAMP gradient, to firstly an enhanced osmotic flow when cAMP is generated intracellularly by addition of ADH and FK, glibenclamide reducing cAMP exit from the cell, and secondly a decreased osmotic flow in response to cAMP (and 8-Br-cAMP) added to the basolateral medium, glibenclamide inhibiting, in this case, their entry into the cell. 2. The demonstration that glibenclamide actually inhibits the basolateral cAMP permeability rests on the fact that firstly it decreases the release of cAMP into the basolateral medium by about 40 %, at each concentration of ADH or forskolin tested, secondly it increases the cAMP content of paired hemibladders incubated in the presence of ADH or FK, when intracellular degradation was prevented by phosphodiesterase inhibition, and thirdly it decreases also the uptake of basolateral 8-Br-[3H]cAMP into paired toad hemibladders. 3. Taken together, the present data demonstrate that glibenclamide inhibits the toad urinary bladder basolateral membrane permeability to cAMP, most probably by a direct interaction with a membrane protein not yet indentified but distinct from the sulphonylurea receptor.

New technique for decorating dislocations in olivine.

Oxidation of iron-rich olivine induced in the laboratory causes preferential precipitation on lattice dislocations. This simple dislocation decoration technique greatly reduces the cost and time involved in surveying the dislocation structures of deformed olivine crystals and opens the way to a more thorough understanding of the deformation of this important geologic material.

Molecular transport in thyroid slices.

The aim of this work is to describe quantitatively, from a physical point of view, molecular, molecular transport in thyroid slices. The study of the release of [3H]sucrose, [3H]inulin and 131I-labeled albumin leads to the following conclusions: the molecular transport in the slices is not due mainly to free diffusion. Indeed as these molecules are retained in the interfollicular spaces, the transport of matter is a mechanical process due to the agitation of the medium in which the slices are incubated. It depends on the elastic properties of the thyroid tissue, the frequency of the agitator and the thickness of the slice. This transport process can be described by a diffusion equation with an empirical diffusion coefficient; we call it diffusivity. These findings must be taken into account in any in vitro kinetic study of thyroid metabolism and of its regulation by effectors such as thyrotropin. The possibility of interference of such mechanical processes in the interpretation of kinetic tracer studies with tissue slices or fragments should be considered.