Effects of targeted disruption of the mouse angiotensin II type 2 receptorgene on stress-induced hyperthermia

We have preciously reported that brain angiotensin II type 2 receptors (AT2 ) contribute to immunological stress-induced hyperthermia (fever) in rats. Now in mice, we report the effect of AT2 gene disruption on the hyperthermi a induced by immunological (interleukin-1 (IL-1) injection) and non-immunol ogical (saline injection or cage switch) stress. 2. AT2-deficient and control mice both showed typical circadian rhythmicity in body temperature and physical activity. During the latter half of the d ark period, AT2-deficient mice exhibited a lower body temperature than the controls. 3. By comparison with the controls, AT2-deficient mice exhibited: (i) a sig nificantly smaller hyperthermia after intraperitoneal (I.P.) injection of I L-1 beta; (ii) significantly greater increases in body temperature and phys ical activity after I.P. saline; and (iii) a significantly greater hyperthe rmia (but a similar increase in activity) during cage-switch stress. 4. These results suggest that AT2, presumably in the brain, plays important roles in stress-induced hyperthermia in mice.