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Evidence that monensin inhibits vasopressin‐stimulated water flow at an early step in the receptor‐adenylate cyclase sequence
Author(s) -
Franki Nicholas,
Mosenkis Bruce,
Hays Richard M.
Publication year - 1989
Publication title -
biology of the cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.543
H-Index - 85
eISSN - 1768-322X
pISSN - 0248-4900
DOI - 10.1111/j.1768-322x.1989.tb00811.x
Subject(s) - monensin , forskolin , cyclase , vasopressin , biology , adenylate kinase , endocrinology , medicine , water flow , receptor , biochemistry , environmental engineering , engineering
Monensin, a highly selective sodium ionophore, inhibits vasopressin‐stimulated water flow in toad urinary bladder pretreated with naproxen, an inhibitor of prostaglandin synthesis. Inhibition is partially dependent on the presence of sodium in the serosal medium, but not on serosal calcium. We have found that monensin does not inhibit water flow generated by forskolin, cyclic AMP, or isobutyl methyl xanthine (MIX); indeed, an enhancement of water flow was seen following cAMP and MIX, as well as following 0.2 μM forskolin. Our findings suggest that monensin uncouples the vasopressin‐receptor‐G protein‐adenylate cyclase sequence at some early step, by a mechanism that remains unknown, but that may directly or indirectlyinvolve intracellular sodium.