Abstract
1. We have previously 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 hyperthermia induced by immunological (interleukin-1 (IL-1) injection) and non-immunological (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 dark period, AT2-deficient mice exhibited a lower body temperature than the controls. 3. By comparison with the controls, AT2-deficient mice exhibited: (i) a significantly smaller hyperthermia after intraperitoneal (i.p.) injection of IL-1beta; (ii) significantly greater increases in body temperature and physical activity after i. p. saline; and (iii) a significantly greater hyperthermia (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.
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