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

摘要

class="enumerated" style="list-style-type:decimal">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.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.By comparison with the controls, AT2-deficient mice exhibited: (i) a significantly smaller hyperthermia after intraperitoneal (i.p.) injection of IL-1β; (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.These results suggest that AT2, presumably in the brain, plays important roles in stress-induced hyperthermia in mice.