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首页> 外文期刊>Journal of Thermal Biology >Arginine vasopressin does not mediate heat loss in the tail of the rat
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Arginine vasopressin does not mediate heat loss in the tail of the rat

机译:精氨酸加压素不介导大鼠尾巴的热量流失

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It has been reported that hypothermia induced by arginine vasopressin (AVP) is brought about by a coordinated response of reduced thermogenesis in brown adipose tissue (BAT) and increased heat loss through the tail of rats. However, it is well known that AVP is one of the strongest peripheral vasoconstrictors. Whether the AVP-induced hypothermia is associated with an increase in heat loss through the tail is questionable. Therefore, the present study assessed the relationship between the effects of AVP on tail skin temperature and the induced hypothermic response, and to determine if peripheral AVP administration increases heat loss from the tail. Core, BAT and tail skin temperature were monitored by telemetry in male Sprague-Dawley rats before and after intraperitoneal administration of AVP or vasopressin receptor antagonist. We also analyzed simultaneously of the time-course of AVP-induced hypothermic response and its relationship with changes in BAT temperature, and effect of AVP on grooming behavior. The key observations in this study were: (1) rats dosed with AVP induced a decrease in heat production (i.e., a reduction of BAT thermogenesis) and an increase of saliva spreading for evaporative heat loss (i.e., grooming behavior); (2) AVP caused a marked decrease in tail skin temperature and this effect was prevented by the peripheral administration of the vasopressin Via receptor antagonist, suggesting that exogenous AVP does not increase heat loss in the tail of rats; (3) the vasopressin V1a receptor antagonist could elevate core temperature without affecting tail skin temperature, suggesting that endogenous AVP is involved in suppression of thermogenesis, but not mediates heat loss in the tail of rats. Overall, the present study does not support the conclusion of previous reports that AVP increased tail heat loss in rats, because AVP-induced hypothermia in the rat is accompanied by a decrease in tail skin temperature. The data indicate that exogenous AVP-induced hypothermia attributed to the suppression of thermoregulatory heat production and the increase of saliva spreading for evaporative heat loss
机译:据报道,精氨酸加压素(AVP)引起的体温过低是由棕色脂肪组织(BAT)的生热减少和大鼠尾部热量流失增加的协同反应引起的。但是,众所周知,AVP是最强的外周血管收缩剂之一。 AVP引起的体温过低是否与通过尾巴的热损失增加有关,这值得怀疑。因此,本研究评估了AVP对尾巴皮肤温度的影响与诱导的低温反应之间的关系,并确定外围AVP给药是否增加了从尾巴排出的热量。在雄性Sprague-Dawley大鼠中,在腹膜内施用AVP或加压素受体拮抗剂之前和之后,通过遥测监测核心,BAT和尾巴皮肤温度。我们还同时分析了AVP引起的低温反应的时程及其与BAT温度变化的关系,以及AVP对修饰行为的影响。这项研究的主要观察结果是:(1)给予AVP的大鼠引起热量产生减少(即BAT热生成减少)和唾液散布增加以蒸发性热量散失(即修饰行为); (2)AVP引起尾巴皮肤温度显着降低,而外周加压素Via受体拮抗剂可防止这种作用,表明外源性AVP不会增加大鼠尾巴的热损失。 (3)加压素V1a受体拮抗剂可以升高核心温度而不影响尾巴皮肤温度,表明内源性AVP参与了生热的抑制,但不介导大鼠尾巴的热损失。总体而言,本研究不支持先前报告得出的结论,即AVP增加大鼠尾部热量流失,因为AVP诱导的大鼠体温过低伴随着尾部皮肤温度降低。数据表明,外源性AVP引起的体温过低归因于温度调节性产热的抑制和唾液散布的增加,以蒸发性热损失

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