Terlouw E M, Kent S, Cremona S, Dantzer R
INRA, Centre de Clermont-Ferrand-Theix, St-Genes-Champanelle, France.
Physiol Behav. 1996 Aug;60(2):417-24.
Vasopressin has been reported to be an endogenous antipyretic peptide. The present study assessed whether this peptide has similar effects on stress-induced hyperthermia. Infusion of 3 ng of vasopressin into the lateral ventricle prior to a 40-min restraint stress reduced significantly the hyperthermic response of rats to this stress, compared to saline-injected controls. Half of the vasopressin-injected animals showed an immediate hypothermic response, with a significant reduction in body temperature of 0.34 degree C or more within 10 min; however, the effect of vasopressin on stress-induced hyperthermia remained significant after exclusion of these animals from the analysis. Administration of a V1 receptor antagonist prior to the stress did not affect the hyperthermic response, which may suggest that the hyperthermic response had reached maximal (ceiling) levels. Administration of vasopressin, or of the V1 receptor antagonist immediately after the stress, did not affect defervescence, suggesting that vasopressinergic systems are not implicated in the defervescence process. Thus, the results show that ICV administration of vasopressin reduces stress-induced hyperthermia. The mechanisms underlying the effects remain to be elucidated.
据报道，血管加压素是一种内源性解热肽。本研究评估了该肽对应激诱导的体温过高是否有类似作用。与注射生理盐水的对照组相比，在40分钟束缚应激前向大鼠侧脑室注入3纳克血管加压素可显著降低大鼠对该应激的体温过高反应。一半注射血管加压素的动物出现即刻体温过低反应，10分钟内体温显著降低0.34摄氏度或更多；然而，在分析中排除这些动物后，血管加压素对应激诱导的体温过高的影响仍然显著。在应激前给予V1受体拮抗剂并不影响体温过高反应，这可能表明体温过高反应已达到最大（上限）水平。应激后立即给予血管加压素或V1受体拮抗剂并不影响退热，这表明血管加压素能系统与退热过程无关。因此，结果表明，脑室内给予血管加压素可降低应激诱导的体温过高。其作用的潜在机制仍有待阐明。
