| Project/Area Number |
11670106
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
General pharmacology
|
|---|
| Research Institution | TOHO UNIVERSITY |
|---|
Principal Investigator |
KOKI Shigenobu Toho University School of Pharmaceutical Sciences Professor, 薬学部, 教授 (50012654)
|
|---|
| Project Period (FY) |
1999 – 2000
|
| Project Status |
Completed (Fiscal Year 2000)
|
| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2000: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1999: ¥2,100,000 (Direct Cost: ¥2,100,000)
|
|---|
| Keywords | mouse myocardium / alpha-adrenergic effect / endothelin / angiotensin I / endocardial endothelium / prostaglandin / action potential / Na+, Ca2+ exchange |
|---|
| Research Abstract |
Research results are summarized as follows.
1) Mechanisms underlying the negative inotropic response to alpha-adrenergic stimulation in adult mouse ventricular myocardium were studied. Results obtained in the present study suggest that the sutained negative inotropic response to alpha-adrenoceptor stimulation of adult mouse ventricular myocardium is mediated by enhancement of Ca2+ efflux through the Na+/Ca2+ exchanger.
2) Alpha-adrenergic stimulation results in a negative inotropic response in adult mouse myocardia as described above, while it produces positive inotropism in neonatal myocardia. Similar developmental conversion of inotropism was observed with endothelin I and angiotensin II ; these agents produced positive response in the neonate but negative in the adult.
3) In mouse left atria, acetylcholine produced a biphasic inotropic response, i.e., a transient decrease in contractile force followed by a late increase. The positive response was found to be mediated by prostaglandin released from the endocardial endothelium.
|
