| Project/Area Number |
09670071
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Environmental physiology (including Physical medicine and Nutritional physiology)
|
|---|
| Research Institution | Yamaguchi University |
|---|
Principal Investigator |
WATANABE Tatsuo Yamaguchi University School of Medicine, Associate Professor, 医学部, 助教授 (60182929)
|
|---|
| Project Period (FY) |
1997 – 1998
|
| Project Status |
Completed (Fiscal Year 1998)
|
| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1998: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1997: ¥2,700,000 (Direct Cost: ¥2,700,000)
|
|---|
| Keywords | Angiotensin II / Angiotensin receptors / Stress / Knockout mouse / Fever / ACTH |
|---|
| Research Abstract |
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.
|
