| Project/Area Number |
03454256
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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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 | KYUSHU UNIVERSITY |
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Principal Investigator |
TAKESHITA Akira Kyushu University, Faculty of Medicine, Professor, 医学部, 教授 (30038814)
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| Co-Investigator(Kenkyū-buntansha) |
KOBAYASHI Sei Kyushu University, Faculty of Medicine, Associate Professor, 医学部, 助教授 (80225515)
IMAIZUMI Tsutomu Kyushu University, Faculty of Medicine, Assistant Professor, 医学部, 講師 (60148947)
砂川 賢二 九州大学, 医学部, 講師 (50163043)
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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 |
¥6,200,000 (Direct Cost: ¥6,200,000)
Fiscal Year 1992: ¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 1991: ¥3,700,000 (Direct Cost: ¥3,700,000)
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| Keywords | borderline hypertensive rat / NaCl / muscimol / shaker stress / sympathetic nerve activity / GABA / muscimol / 食塩 / 境界型高血圧 / ストレス / ムシモ-ル / ビククリン / 脳室内投与 |
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| Research Abstract |
We aimed to determine 1) if high salt diet augments the pressor response to shaker stress in borderline hypertensive rats (BHR) and 2) if ICV muscimol attenuates the augmented pressor response to shaker stress in high-salt BHR. The studies were done in conscious BHR and WKY of the two groups (high and normal salt diet for 5 weeks). The results demonstrated the following findings : 1) high salt intake increased resting arterial pressure and augmented pressor response to shaker stress in BHR but not in WKY, 2) ICV muscimol caused a greater decrease in mean arterial pressure and renal sympathetic nerve activity in BHR-NaCl than in BHR-control, 3) ICV muscimol attenuated the pressor response to shaker stress dose-dependently in BHR-NaCl but did not alter it in BHR-control or in WKY, and 4) Resting mean arterial pressure and the pressor response to shaker stress in BHR-NaCl after ICV muscimol did not differ form those in BHR-control. These results suggest that high salt intake may reduce the sympathetic inhibitory effect of central GABA system, which may contribute to salt-induced hypertension and the augmented response to stress in BHR.
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