Role of angiotensin II type 2 receptors in the development of stress-induced hyperthermia in mouse : a knockout mouse study

我们研究了血管紧张素II型2受体（AT_2）基因破坏对免疫[白介素-1 （IL- 1）注射]和非免疫（盐水注射或换笼）应激引起的高热的影响。在黑暗时期，at_2缺陷小鼠和对照组小鼠的体温和体力活动都有所增加。在黑暗时期，at_2缺陷小鼠的体温低于对照组。腹腔注射il -1 β后，at_2缺陷小鼠的高热程度明显低于对照组。与对照组相比，at_2缺陷小鼠在接受生理盐水或换笼应激后体温明显升高。提示AT_2在小鼠应激性热疗中起重要作用。

We investigated the effect of angiotensin II type 2 receptor (AT_2)-gene disruption on the hyperthermia induced by immunological [Iinterleukin-1 (IL- 1)-injection] and non-immunological (saline-injection or cage-switch) stress. AT_2-deficient and control mice showed increases in body temperature and physical activity during dark period. AT_2-deficient mice exhibited a lower body temperature than the controls during the dark period. AT_2-deficient mice showed a significantly smaller hyperthermia than the controls after intraperitoneal (i.p.) injection of IL-1beta. By comparison with the controls, AT_2-deficient mice had significantly greater increases in body temperature after i.p. saline or during cage-switch stress. These results suggest that AT_2 plays important roles in stress-induced hyperthermia in mice.