Ethanol (9%) decreases the potential difference across the toad bladder when present at the mucosal surface, the short circuit current was unchanged. The electrical resistance decreased indicating a change in ion movements across the bladder. Unidirectional 22Na and 36Cl flux measurements showed an increase in the movement of Cl, but no change in Na. The vasopressin induced increase in Na transport (natriferic response) was also unaffected by the presence of ethanol. It is suggested that ethanol may be altering the apical tight junctions and affecting an anion selective pathway. The hydro osmotic response of the toad bladder to vasopressin was decreased by 70% in the presence of 3% ethanol. The hydro osmotic action of cyclic adenosine monophosphate was also inhibited by ethanol, indicating an action subsequent to the endogenous formation of this nucleotide. Tritiated water fluxes (in the absence of an osmotic gradient) were reduced by 30% in the presence of 3% ethanol. The vasopressin induced increase in diffusional water flow was similarly reduced. Osmotic water movements across glutaraldehyde and N ethylmaleimide 'fixed' vasopressin stimulated bladders were also decreased in the presence of ethanol. However, 3% ethanol had no effect on osmotic water transfer across artificial collodion membranes. Ethanol, therefore, probably interacts with the bladder membrane. The K(trans) (permeability coefficient) of ethanol and water is increased by vasopressin, suggesting that their movement is through similar pathways. It is suggested that ethanol impedes the flow of water across the toad bladder by facilitating a physicochemical interaction between the membrane 'pore' and the water molecules.
|Number of pages||11|
|Journal||Journal of Pharmacology and Experimental Therapeutics|
|State||Published - 1 Dec 1976|