| Project/Area Number |
09470008
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | Gifu University |
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Principal Investigator |
MORITA Hironobu Gifu University, School of Medicine, Physiology, Professor, 医学部, 教授 (80145044)
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| Co-Investigator(Kenkyū-buntansha) |
WATANABE Kazuko Gifu University, School of Medicine, Physiology, Associate Professor, 医学部, 講師 (40158621)
LEE Ken Gifu University, School of Medicine, Physiology, Associate Professor, 医学部, 助教授 (00212316)
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| Project Period (FY) |
1997 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥7,600,000 (Direct Cost: ¥7,600,000)
Fiscal Year 1999: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1998: ¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 1997: ¥3,700,000 (Direct Cost: ¥3,700,000)
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| Keywords | hepatoportal NaィイD1+ィエD1 and KィイD1+ィエD1 receptors / NaィイD1+ィエD1 and KィイD1+ィエD1 homeostasis / NaィイD1+ィエD1 KィイD1+ィエD1 2ClィイD1-ィエD1 contransporter / urinary NaィイD1+ィエD1 and KィイD1+ィエD1 excretion / hepatic nerve / central projection / Fos protein / bumetanide / 門脈-肝臓領域Na^+受容器 / 門脈-肝臓領域K^+受容器 / Na^+K^+2Cl^-共輸送体 / K^+恒常性維持 / 尿中K^+排泄 / 肝臓除神経 / ブメタナイド / Hepatic nerve / Na^+K^+2Cl^- cotransporter / Bumetanid / Na^+ receptor / K^+ receptor / Kaliuresis / 門脈-肝臓領域Na受容機構 / 孤束核 / 第3脳室周囲核 / 視策上核 / Naバランス / 食塩嗜好性 |
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| Research Abstract |
Recently, we demonstrated that the hepatoportal NaィイD1+ィエD1-sensitive mechanism plays a significant role in maintaining body fluid homeostasis by controlling renal excretory and jejunal absorptive functions. The afferent pathway of the hepatic body fluid control system is the periarterial hepatic nerve and efferent pathways are the renal sympathetic nerve and cholinergic fibers to the jejunum. However the sensor mechanisms and central pathways are still unknown. Accordingly, the purposes of the present study was to examine these two points and the following conclusions were obtained:
(1) The hepatoportal NaィイD1+ィエD1-receptive signals projects to the brain stem, hypothalamus, and forebrain structures involved in autonomic function and osmoregulation, then activate the fluid-regulatory mechanism. However, the hepatoportal osmoreceptive signals do not activate these central structures.
(2) The hepatoportal NaィイD1+ィエD1 receptor senses the NaィイD1+ィエD1 concentration via the bumetanide-sensitiv
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e NaィイD1+ィエD1 KィイD1+ィエD1 2ClィイD1-ィエD1 cotransporter.
(3) The hepatoportal bumetanide-sensitive NaィイD1+ィエD1 KィイD1+ィエD1 2ClィイD1-ィエD1 cotransporter also participate in the KィイD1+ィエD1-sensitive mechanism. When this mechanism is stimulated, kaliuresis occurs via the periarterial hepatic nervous plexus. Thus, the hepatoportal bumetanide-sensitive KィイD1+ィエD1-sensor mechanism may play an important role in regulating extracellular KィイD1+ィエD1 homeostasis.
The hepatoportal NaィイD1+ィエD1- and KィイD1+ィエD1-sensor mechanisms would be triggered by an increase in the portal venous NaィイD1+ィエD1 and KィイD1+ィエD1 concentrations in advance of changes in the systemic blood NaィイD1+ィエD1 and KィイD1+ィエD1 concentrations and reflexively regulate NaィイD1+ィエD1 and KィイD1+ィエD1 excretion. The important feature of this system is that the portal venous blood flow is 20〜25 % of cardiac output and the concentration of ions and the changes therein are therefore 4-5-times greater than in the systemic circulation. If the purpose of this system is to regulate the systemic blood NaィイD1+ィエD1 and KィイD1+ィエD1 concentrations, but not the portal venous NaィイD1+ィエD1 and KィイD1+ィエD1 concentrations, it would be operated by predicting the systemic blood concentrations from the portal venous concentrations and such prediction can result in errors of regulation. This control error would be corrected by other negative feedback systems. Less
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