| Project/Area Number |
63480121
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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 |
General pharmacology
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| Research Institution | Fukuoka University |
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Principal Investigator |
FURUKAWA Tatsuo School of Medicine, Department of Pharmacology, Professor, 医学部, 教授 (60078582)
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| Co-Investigator(Kenkyū-buntansha) |
SHIBATA Kazuhiko School of Medicine, Research Laboratory of Biodynamics, Instructor, 医学部, 助手 (80170893)
山田 勝士 福岡大学, 医学部, 助教授 (00037491)
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| Project Period (FY) |
1988 – 1990
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥5,000,000 (Direct Cost: ¥5,000,000)
Fiscal Year 1990: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1989: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1988: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Central control / Brain sites / Blood pressure / Fluid intake / Angiotensin / GABA / taurine / atrial natriuretic peptide / アンギオテンシンII / 心房性ナトリウム利尿ペプチド / 視索前野 / 高血圧自然発症ラット / 高血圧 / 後部視床下部 |
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| Research Abstract |
The experiments were undertaken in un-anesthetized and freely moving rats. 1)Renin and angiotensin II(AII)administered into the cerebroventricle caused pressor responses via stimulating AII receptors, which was potentiated in spontaneously hypertensive rats(SHR)than those in control Wistar Kyoto rats(WKY). 2)AII receptors involved in central pressor responses are found in the preoptic area(POA)and suprachiasmatic nucleus, but not in the central amygdaloid nucleus and paraventricular nucleus. The pressor responses are potentiated in SHR at only POA, and this hyperresponsiveness seems to be involved in not evocation but maintenance of hypertension, on the basis of differences between 6 and 15 weeks SHR. Pressor responses to AII are antagonized by central administration of GABA or taurine. The antagonism is not mediated by directly acting on POA, but by indirectly acting on other brain sites. 3)AII induced not only pressor responses but also an increase of water and salt intake, which are also potentiated in SHR. For this potentiation in fluid intakes, POA is also importantly involved. These responses to AII are antagonized by atrial natriuretic peptide(ANP)at POA and posterior hypothalamus(PH)in SHR but not in WKY, indicating responsiveness to ANP is also potentiated in SHR at those areas. The results suggest that the activities of brain AII and ANP neuronal system may play an important role in central controlling the cardiovascular system at POA and PH and is altered at these areas in genetically hypertensive rats.
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