Effect of metabolic inhibitors on vasopressin-stimulated transport systems in the toad bladder

✍ Scribed by Hays, Richard M. ;Franki, Nicholas ;Ross, Lawrence S.

• Publisher: Wiley (John Wiley & Sons)
• Year: 1979
• Tongue: English
• Weight: 638 KB
• Volume: 10
• Category: Article
• ISSN: 0091-7419
• DOI: 10.1002/jss.400100207

✦ Synopsis

Vasopressin increases the permeability of receptor cells t o water and, in tissues such as toad bladder, t o solutes such as urea. While cyclic AMP appears t o play a major role in mediating the effects of vasopressin, there is evidence that activation of the water permeability system and the urea permeability system involves separate pathways. In the present study, we have shown that inhibitors of oxidative metabolism (rotenone, dinitrophenol, and methylene blue) selectively inhibit either vasopressin-stimulated water flow or vasopressin-stimulated urea transport. There was no inhibition, however, when exogenous cyclic AMP was substituted for vasopressin, and little t o no inhibition when the potent analogue 8-bromoadenosine 3',5'-cyclic monophosphate (8-Br-CAMP) was employed. Rotenone had no effect on adenylate cyclase activity or cyclic AMP levels within the cell; dinitrophenol decreased adenylate cyclase activity minimally.

tubule assembly, demonstrated an inhibition of vasopressin and cyclic AMPstimulated water flow but showed no effect on urea transport. stimulated processes, have different links t o cell metabolism, and that in addition t o cyclic AMP, a non-nucleotide pathway may be involved in the action of vasopressin.

Additional studies with vinblastine and nocodazole, inhibitors of micro-We would conclude that water and urea transport, as examples of hormone-