| Project/Area Number |
04807063
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Yokohama City University |
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Principal Investigator |
SHIONOIRI Hiroshi Yokohama City University, School of Medcine, Associate Prof., 医学部, 講師 (20128599)
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| Co-Investigator(Kenkyū-buntansha) |
TAKASAKI Izumi Yokohama City University, School of Medicine, Assistant Prof., 医学部, 助手 (00244492)
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| Project Period (FY) |
1992 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1994: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1993: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1992: ¥800,000 (Direct Cost: ¥800,000)
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| Keywords | Atherosclerosis, / Hypertension, / Vascular diseases, / Fibronectin, / Growth factors |
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| Research Abstract |
Effects of hypertension and aging on aortic fibronectin expression were investigated in male Dahl salt-sensitive (Dahl-S) and salt-resistant (Dahl-R) rats fed either a low or high salt diet from 5 to 37 weeks of age. In comparison to low salt controls, the steady state mRNA levels for aortic fibronectin in salt-loaded Dahl-S rats were dramatically increased at 37 weeks of age, corresponding to a severe stage of hypertension with high mortality, while at earlier ages representing early to established phases of hypertension, no significant changes were observed. Saltloading affected neither blood pressure nor aortic fibronectin expression in Dahl-R rats. Aging without coexisting hypertension did not cause significant changes in aortic fibronectin mRNA levels all through the study period in either strain of rats. These results suggest that aortic fibronectin may be strongly regulated by factors associated with severe hypertensive organ damages caused by long-standing hypertension in saltloaded Dahl-S rats. Also suggested was that aortic fibronectin may not play a major role in the pathogenesis of early aortic changes occurring in response to hypertension or as a process of aging.
As an extension of the above experiments, isolated arteries were dilated by the balloon angioplasty catheter, resulting in an increased induction of a proto-oncogene (c-fos) without increase in fibronectin mRNA.This in vitro experimental system is expected to provide clues to understand the mechanism of gene regulation related with aortic fibronectin expression and aortic wall hypertrophy.
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