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Elsevier Science

Brain Res. 1990 Apr 02;512(2):243-7. doi: 10.1016/0006-8993(90)90632-l.

The effectiveness of arginine vasopressin and sodium salicylate as antipyretics in the Brattleboro rat.

Brain research

D M Fyda, W B Mathieson, K E Cooper, W L Veale

Affiliations

  1. Department of Medical Physiology, Faculty of Medicine, University of Calgary, Alta., Canada.

PMID: 2354361 DOI: 10.1016/0006-8993(90)90632-l

Abstract

The infusion of either 30 micrograms/microliters (approx. 100 micrograms/kg/h) of sodium salicylate or 10 ng/microliters (10(-5) M) arginine vasopressin within the ventral septal area of the Brattleboro rat brain reduced a centrally induced prostaglandin E1 (PGE1) hyperthermia when compared with infusions of artificial cerebrospinal fluid. Conversely, the infusion of a related peptide, oxytocin (10 ng/microliters (10(-5) M), or 33 ng/kg/h) failed to alter the rise in core temperature following the PGE1 injection. These results suggest that the vasopressin receptors reported to be present in the Brattleboro rat may respond normally to exogenously administered vasopressin, thus allowing for the antipyretic action. Moreover, the antipyretic effects of sodium salicylate suggest that aspirin-like drugs may induce the release of alpha-melanocyte-stimulating hormone which, in turn, attenuates the PGE1-evoked fever. Given recent evidence, however, which suggests that the Brattleboro rat may contain vasopressin both peripherally and within the brain, the antipyretic action of sodium salicylate may be alternatively explained through the endogenous release of vasopressin.

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