Abstract
Acetylsalicylic acid by itself has no effect on net water movement but clearly potentiates the response to oxytocin and to an increase in medium tonicity in toad urinary bladder. No interaction was observed between the tested drug and exogenous adenosine 3′:5′-monophosphate. The hypothesis that the control mechanism based on cellular osmolarity as previously described is operated via the liberation of prostaglandin E 1 is suggested.
Published Version
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