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Pflügers Archiv

, Volume 413, Issue 5, pp 451–455 | Cite as

Sodium salicylate: alternate mechanism of central antipyretic action in the rat

  • Susan J. Alexander
  • Keith E. Cooper
  • Warren L. Veale
Heart, Circulation, Respiration and Blood; Environmental and Exercise Physiology

Abstract

Infusion of sodium salicylate (50.0 or 100.0 μg/μl) into the ventral septal area (VSA) of the rat brain suppressed Prostaglandin-E1-induced hyperthermia. Infusion of artificial cerebrospinal fluid (aCSF) or 10.0 μg doses of salicylate did not. The suppression of intracerebroventricularly-induced (icv) Prostaglandin E1 (PGE1) hyperthermia was not due to a hypothermic action of salicylate since salicylate infusions given during cold exposure (10.0°C) did not lower core body temperatures. A possible interaction between salicylate and endogenous arginine vasopressin (AVP) was investigated. Infusion of both salicylate (50.0 μg/μl) and either AVP antiserum or AVP antagonist into the VSA resulted in PGE hyperthermias occurring at levels which were not different from control levels as opposed to enhanced hyperthermia (antiserum or antagonist alone) or suppressed hyperthermia (salicylate alone). These results are consistent with the notion that sodium salicylate infusions within the VSA enhance AVP action and thus bring about the attenuation of PGE-induced hyperthermia.

Key words

Sodium salicylate Arginine vasopressin Fever Prostaglandin E Central nervous system ventral septal area Hyperthermia 

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Copyright information

© Springer-Verlag 1989

Authors and Affiliations

  • Susan J. Alexander
    • 1
  • Keith E. Cooper
    • 1
  • Warren L. Veale
    • 1
  1. 1.Department of Medical Physiology, Faculty of MedicineThe University of CalgaryCalgaryCanada

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