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- W2071247440 abstract "The antihypertensive drugs guanabenz and clonidine have been shown to produce water diuresis. Decreased release of vasopressin (ADH) and reduced tubular Na transport may contribute to the diuretic effect, but a cellular antagonism of ADH has not been excluded. We examined in toad bladders the ability of guanabenz and clonidine to antagonize the increase in osmotic water flow (Jv) which was stimulated by ADH. Guanabenz (1 × 10−8 to 10−6 M) decreased ADH-stimulated Jv but not basal Jv. Its primary metabolite had no effect. Clonidine inhibited ADH-stimulated Jv less than guanabenz. The effect of guanabenz was abolished by phenoxybenzamine and yohimbine but not by naproxen or prazosin. Phenylephrine, an α1-agonist, decreased ADH-stimulated Jv onlyt or above 1 × 10−5M. Guanabenz was about 10-fold less potent an inhibitor of 14C-urea flux than of osmotic water flow and did not affect short circuit current. These studies suggest that postsynaptic α2-adrenoceptors may modulate the action of ADH to increase water permeability of the toad bladder." @default.
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- W2071247440 date "1980-12-01" @default.
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- W2071247440 title "Antagonism of the hydrosmotic effect of vasopressin by the antihypertensive, guanabenz" @default.
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- W2071247440 doi "https://doi.org/10.1016/0024-3205(80)90531-7" @default.
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