| Project/Area Number |
01870041
|
|---|
| Research Category |
Grant-in-Aid for Developmental Scientific Research
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Circulatory organs internal medicine
|
|---|
| Research Institution | Hokkaido University |
|---|
Principal Investigator |
KAWAGUCHI Hideaki Hokkaido University School of Medical Hospital Faculty, 医学部附属病院, 助手 (70161297)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
OIKAWA Tsuneyuki Sasaki Cancer Inst, Chief, 部長 (80150241)
YASUDA Hisakazu Hokkaido University School of Medicine professor, 医学部, 教授 (20010126)
|
|---|
| Project Period (FY) |
1989 – 1990
|
| Project Status |
Completed (Fiscal Year 1990)
|
| Budget Amount *help |
¥18,300,000 (Direct Cost: ¥18,300,000)
Fiscal Year 1990: ¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 1989: ¥14,900,000 (Direct Cost: ¥14,900,000)
|
|---|
| Keywords | Inositolphosphate / Calcium / Phospholipase c / Signal transduction / イノシト-ル4リン酸 / ホスホリパ-ゼC / 細胞内カルシュウム / IP4 / IP3 / ホスフォリパ-ゼC |
|---|
| Research Abstract |
Objective : Free cytosolic calcium plays an important role in the development of cell proliferation. Inositol 1,4,5-trisphosphate (IP3) is a second messenger releasing intracellular Ca^<2+> into the cytosol from sarcoplasmic reticulum (SR). We determined Ca^<2+> release from SR stimulated by IP3 in hypertrophied rat heart to investigate the relationship between cardiac hypertrophy and Ca^<2+>
Design and Methods : Experiments were carried out on 10-30-week-old male spontaneously hypertensive rat (SHR) and age-matched normotensive Wistar-kyoto rat (WKY). Rat heart was homogenized and centrifuged at 105,000xg for 90 min. The resultant pellets were used as SR fraction. SR fractions were also obtained from SHR treated with alpha 1-blockade, bunazisin-HC1 (10 mg/Kg body weight/day) or beta-blockade, atenolol (20 mg/Kg body weight/day)
Results : Ca^<2+> release stimulated by IP3 was detected at 1 M of IP3. The release was dose dependently increased by 5 M or IP3. The release was higher in 10-30 weeks old SHR compared with agematched WKY.Left ventricular weight was markedly decreased in SHR treated with alpha- or beta-blockade. Ca^<2+> release stimulated with IP3 was also suppressed in these SHR treated with antihypertensive drugs, significantly. Now we have been trying to purify IP4 binding protein.
Conclusion : These results may suggest that IP3 and Ca^<2+> have an important role in cardiac hypertrophy in SHR.
|
