| Project/Area Number |
09670725
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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 | KYUSHU UNIVERSITY |
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Principal Investigator |
OHYA Yusuke Faculty of Medicine, KYUSHU UNIVERSITY Assistant Professor, 医学部, 助手 (30240964)
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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 |
¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1998: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1997: ¥800,000 (Direct Cost: ¥800,000)
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| Keywords | Vascular smooth muscle / Hypertension / SHR / Channel / イオンチャンネル |
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| Research Abstract |
The arteria] wall is continuously exposed to mechanical stresses such as shear stress and lumial pressure. It is known that mechanical stress caused various biological responses in the arterial wall, However, the machanisms by which signal transduction from mechanical stimuli to intracellular factors occur are not fully understood. We evaluated the stretch-activated (SA) channels in vascular smooth muscle cells by using patch clamp technique. The SA channels were activated by mechanical stress (stretch of the membrane) and allowed Ca^<2+> and Na^+ into the cell. The ion fluxes per se and the following membrane depolarization would cause the cell excitation. The Gd^<3+>, a known specific blocker of SA channels, inhibited SA channels and L-type Ca^<2+> channel with a similar potency in vascular smooth muscle cells. We thus consider that Gd^<3+> is not a specific blocker of SA channels in vascular smooth muscle cells.
Electricalan d contractile responses of samll arteries to mechanical stress are reportedly enhanced in spontaneously hypertensive rats (SHR), conpared with WKY rats. We comared SA channels in vascular smooth muscle cells from SHR and WKY.We showed that the activation of SA channels were enhanced in SHR cells.
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