| Project/Area Number |
13670059
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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 |
Environmental physiology (including Physical medicine and Nutritional physiology)
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| Research Institution | University of Yamanashi (Faculty of Medicine) |
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Principal Investigator |
SAIGUSA Takeshi University of Yamanashi ,Faculty of Medicine, Assistant Professor, 医学部, 講師 (70215523)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2002: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2001: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | Angiotensin / Baroreflex / Ventrolateral Medulla / Sympathetic Nerve Activity / Cardiovascular Neuron / Single-Unit Recording / Rabbit / Automatic Control / アンギオテンシンII / 交感神経系 / 細胞外記録法 / レーザー変位計 / 交感神経 / 血管運動ニューロン / 細胞外記録 / 麻酔 |
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| Research Abstract |
Fourth-ventricular (4V) administration of angiotensin II (Ang II) facilitates renal sympathetic baroreflex in rabbits. The aim of the present study is to identify the site(s) of this Ang II action and to clarify its neuronal mechanism.
1. Identifying the site of action
The renal sympathetic baroreflex facilitation induced by 4V Ang II (10 pmol/min) was completely blocked by a pretreatment of bilateral rostral ventrolateral medulla (RVLM) with an Ang II receptor antagonist (Sarile, 10 pmol). The result strongly suggests that the RVLM is the major site of action mediating the 4V Ang II-induced baroreflex facilitation.
2. Development of a unit-recording system
A new recording system was developed for the purpose of recording single-unit activities from the medullary cardiovascular neurons during baroreflex analysis. The system consists of a carbon-fiber floating electrode and an electrode tracking-control device that compensates brain dislocation induced by blood pressure manipulation.
3. Clarifying the neuronal mechanism
The effects of Ang II on the blood pressure-activity relationship of the RVLM cardiovascular neurons were investigated. In half of the cardiovascular neurons investigated, Ang II increased the upper limit of neuronal activation in response to a decrease in blood pressure. Average curves before and after the Ang II administration were reconstructed from the individual blood pressure-activity relationships. The average curves were qualitatively identical with the renal sympathetic baroreflex curves before and after 4V Ang II. The result suggests that the 4V Ang II-induced sympathetic baroreflex modulation is attributed to the effects of Ang II on the blood pressure-activity relationship in the RVLM cardiovascular neurons.
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