Project/Area Number |
26460909
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General internal medicine(including psychosomatic medicine)
|
Research Institution | Kochi University |
Principal Investigator |
SHIMIZU Takahiro 高知大学, 教育研究部医療学系基礎医学部門, 准教授 (00363276)
|
Co-Investigator(Kenkyū-buntansha) |
清水 翔吾 高知大学, 教育研究部医療学系基礎医学部門, 助教 (90721853)
中村 久美子 高知大学, 教育研究部医療学系基礎医学部門, 技術専門職員 (30398052)
田中 健二朗 高知大学, 教育研究部医療学系基礎医学部門, 助教 (30552260)
八幡 俊男 高知大学, 教育研究部医療学系臨床医学部門, 助教 (40380323)
東 洋一郎 高知大学, 教育研究部医療学系基礎医学部門, 助教 (80380062)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
|
Keywords | 脳内大麻 / エンドカンナビノイド / CB受容体 / 自然発症高血圧ラット / 高血圧症 / 交感神経-副腎髄質系 / 脳内麻薬 / オピオイド受容体 / 中枢性交感神経―副腎髄質系 / オピオイド / μ受容体 |
Outline of Final Research Achievements |
The sympatho-adrenomedullary (SA) system is an important component of responses to stress, and it has recognized that excessive activation of this system plays a pathogenic role in triggering and sustaining the essential hypertension. We have already reported an inhibitory role of brain endocannabinoid (eCB) in stress-related neuropeptides-induced activation of the SA outflow via brain CB1 receptors. In this study, we clarified that (1) stimulation of brain CB1 receptors improved excessive hypertension and activation of the outflow in spontaneously hypertensive rats without affecting these factors in normotensive control rats, and that (2) brain opioid receptors, which can interact with CB1 receptors, modulate these peptides-induced activation of the SA outflow. These findings suggest that brain CB1 and opioid receptors might be useful targets for alleviation of essential hypertension via inhibition of stress responses including the SA outflow.
|