| Project/Area Number |
09670039
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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 |
General physiology
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| Research Institution | St.Luke's College of Nursing |
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Principal Investigator |
KUMADA Mamoru St.Luke's College of Nursing, Professor, 看護学部, 教授 (00110487)
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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 |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1998: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1997: ¥2,700,000 (Direct Cost: ¥2,700,000)
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| Keywords | power spectrum / blood pressure / electrocardiograph / sympathetic nervous system / cardiac vagus nerve / endothelin-1 gene knockout mouse / endothlein B receptor gene knockout mouse / ryanodine type3 receptor gene knockout mouse / エンドセリン-1 遺伝子欠損マウス / ノックアウトマウス / 遺伝子過剰発現マウス / 自律神経 / 収縮期血圧 / 迷走神経 |
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| Research Abstract |
I investigated whether the power spectral analysis of blood pressure and heart rate variability, when applied to the mouse, gave useful information on the autonornic nervous control of the circulation. I found that the autoregression method is suitable for this purpose, but that the drift of the baseline had to be effectively removed. The power spectrum thus calculated was characterized by the low (LF) and high frequency components (HIF). By means of pharmacological experiments, I confirmed that both LF and HF represented either sympathetic or parasympathetic component of the autonomic nerve activity. The LF component of systolic arterial pressure (SAP) variability corresponded to activity of sympathetic vasoconstrictor nerve, whereas the LF of heart rate variability represented activity of the cardiac sympathetic nerve. The HF of heart rate variability corresponded to activity of the cardiac vagus nerve. I subsequently applied the power spectral analysis to three types of knockout mice. The knockout mouse with the disrupted endothelin gene (ET-l knockout mouse) showed lower blood pressure by about 10 mmHg as compared to wild type counterparts. Both LF and HF of SAP variability were augmented in ET- 1 knockout mouse indicating elevated activity of sympathetic vasomotor nerve underlay higher blood pressure. In those knockout mice whose endothelin B (ETB) receptors were 1/8 of wild time mice (ETB knockout mice) exhibited higher blood pressure by 20 mmHg than their wild type counterparts. However, no difference m LF and HF were found between the two groups suggesting that high blood pressure of ETB knockout mice was not of neurogenic but peripheral origin. Finally, the knockout mouse lacking ryanodine type 3 receptors showed an increased heart rate and diminished LF and HF of heart rate variability. It is suggested that decrease in cardiac vagal activity caused this bradycardia.
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