| First Author | Watanabe T | Year | 1999 |
| Journal | J Physiol | Volume | 515 ( Pt 3) |
| Pages | 881-5 | PubMed ID | 10066912 |
| Mgi Jnum | J:54821 | Mgi Id | MGI:1336092 |
| Doi | 10.1111/j.1469-7793.1999.881ab.x | Citation | Watanabe T, et al. (1999) Effects of targeted disruption of the mouse angiotensin II type 2 receptor gene on stress-induced hyperthermia. J Physiol 515 ( Pt 3):881-5 |
| abstractText | 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. |
