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pubmed-article:2528390pubmed:abstractTextInfusion of 15 micrograms/microliters (approximately 120 micrograms/kg/h) of indomethacin within the ventral septal area of the rat brain significantly reduced a centrally induced prostaglandin E1 (PGE1) hyperthermia when compared with infusions of artificial cerebrospinal fluid. A bolus injection of a V1 receptor antagonist, d(CH2)5Try(Me)AVP, (200, 2000, or 20,000 pmol) within the ventral septal area had no effect of body temperature alone but did suppress the PGE1-induced fever. Similar bolus injections of the V1 receptor antagonist within the ventral septal area failed to alter the antipyretic action of indomethacin on the hyperthermia resulting from centrally administered PGE1. Central injections of a V2 receptor antagonist failed to alter either the PGE1-induced fever or the indomethacin-evoked antipyresis. The results suggest that the V1 receptor antagonist may exert non-specific neurodepressant effects which may interfere with the expression or production of PGE1 hyperthermia and may further mask any contribution of arginine vasopressin to the antipyretic effects of indomethacin.lld:pubmed
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pubmed-article:2528390pubmed:dateRevised2010-11-18lld:pubmed
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pubmed-article:2528390pubmed:articleTitleIndomethacin-induced antipyresis in the rat: role of vasopressin receptors.lld:pubmed
pubmed-article:2528390pubmed:affiliationDepartment of Medical Physiology, Faculty of Medicine, University of Calgary, Alta., Canada.lld:pubmed
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pubmed-article:2528390pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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