| Project/Area Number |
09670740
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Wakayama Medical Collage |
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Principal Investigator |
UEYAMA Takashi Wakayama Medical Collage, Assistant professor, 医学部, 講師 (50264875)
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| Co-Investigator(Kenkyū-buntansha) |
SENBA Emiko Wakayama Medical Collage, Professor, 医学部, 教授 (00135691)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 1998: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1997: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Emotional stress / Heart / Electrocardiogram / Immediate early genes / Natriuretic peptide / Heat shock protein / Adrenoceptor / Signal transduction / Emotional stress / Heart / Electrocardiogram / Immediate early genes / ANP / HSP70 / Adrenoceptor / cross-talk / emotional stress / immediate early genes / BNP / HSP / αβ-blocker / vasospastic angina |
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| Research Abstract |
Emotional stress, and associated activation of adrenergic system underlie cardiac accidents. Immobilization stress of rats, which produces activation of the sympatho-adrenal medullary system, induced ischemic electrocardiographic changes. Corresponding to these changes, immediate early genes/transcriptional factors (IEGs) were expressed in the smooth muscle cells of coronary arteries, enodothelial cells and myocardium. Furthermore, mRNA for heat shock protein 70 was induced in the aortic and coronary smooth muscles cells from 30min to 3h after onset of stress. Natriuretic peptide genes (ANP and BNP) were also upregulated. Sequential expression of these genes can be considered as an adaptive response to stress. Not a single but synergistic blocking of alpha and beta adrenoceptors blocked the IEGs expressions elicited by stress. Either alpha or beta agonist upregulated IEGs in the perfused heart. Activation of alpha or beta adrenoceptors is the primary trigger of stress-induced molecular and electrophysiological changes in the heart. Crosstalk of signal transduction between downstream of alpha and beta adrenoceptors in these cardiac cells is also suggested.
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