| Project/Area Number |
03670469
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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 | Hyogo College of Medicine |
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Principal Investigator |
OHYANAGI Mitsumasa Hyogo College of Medicine, Dept.of Medicine, lecturer, 医学部, 講師 (90131573)
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| Project Period (FY) |
1991 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1992: ¥200,000 (Direct Cost: ¥200,000)
Fiscal Year 1991: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | alpha-adrenoceptor / subtype / microcirculation / SHR / myogenic response / in vitro / myogenic response / αーadrenergic receptor |
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| Research Abstract |
Hyperresponsiveness of vascular smooth muscle to alpha-AR-mediated vasoconstriction has been proposed as a factor involved in maintenance of the elevated vascular resistance in hypertensive state. alpha AR constriction can be mediated by two types of alpha-AR, alpha-1 and alpha-2. No conclusive evidence has been demonstrate in which subtype of alpha-AR playesmainly the role on maintenance of peripheral resistance in hypertensive rats (SHR). The sensitivity of alpha-AR of resistance large arteriole was examined with in vitro videomicroscopy in prehypertensive(4-5 week) and early hypertensive stage(7-8 week) of SHR compared with age mayched WKY. Microdissected vessels were double-cannulated with glass micropipets in a tissue bath. Norepinephrine (NE) concentration-response curves were obtained in the presence of prazosine or rauwolscine to establish the concentrations of NE required to selectivity stimulate alpha-1 or alpha-2 AR. The sensitivity to alpha-1 constriction was much greater in SHR than WKY in both stage. There was no difference in alpha-2 constriction between SHR and WKY. We also examined to explore which alpha subtype has a greater sensitivity to myogenic modulation in SHR. Myogenic constriction during in lumen pressure was greater during alpha-2 than alpha-1. These finding suggested that hypersensitivity of alphaAR to vasoconstriction play a role on maintenance or etiologic factor in elevated vascular resistance in hypertension.
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