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ヒトレニン, ヒトアンギオテンシノーゲン両遺伝子を導入した高血圧モデルマウスの作成ならびに血圧上昇機序の解析
https://kindai.repo.nii.ac.jp/records/2002048
https://kindai.repo.nii.ac.jp/records/2002048aa6ee13a-63ff-4d6e-a96d-3b92c99713ad
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
AN00063584-19931225-0579.pdf (911.8 KB)
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| Item type | ☆紀要論文 / Departmental Bulletin Paper(1) | |||||||||
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| 公開日 | 2024-11-22 | |||||||||
| タイトル | ||||||||||
| タイトル | ヒトレニン, ヒトアンギオテンシノーゲン両遺伝子を導入した高血圧モデルマウスの作成ならびに血圧上昇機序の解析 | |||||||||
| 言語 | ja | |||||||||
| タイトル | ||||||||||
| タイトル | Generation and analysis of hypertensive transgenic mice carrying both human renin and human angiotensinogen genes | |||||||||
| 言語 | en | |||||||||
| 著者 |
杉村, 圭一
× 杉村, 圭一
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| 言語 | ||||||||||
| 言語 | jpn | |||||||||
| キーワード | ||||||||||
| 主題 | Renin-angiotensin system, Hypertension, Transgenic mice | |||||||||
| 資源タイプ | ||||||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||||||
| 資源タイプ | departmental bulletin paper | |||||||||
| 出版タイプ | ||||||||||
| 出版タイプ | AM | |||||||||
| 出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||||||
| 出版者 名前 | ||||||||||
| 出版者 | 近畿大学医学会 | |||||||||
| 言語 | ja | |||||||||
| bibliographic_information |
ja : 近畿大学医学雑誌 en : Medical Journal of Kinki University 巻 18, 号 4, p. 579-592, 発行日 1993-12-25 |
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| ISSN | ||||||||||
| 収録物識別子タイプ | PISSN | |||||||||
| 収録物識別子 | 03858367 | |||||||||
| 内容記述 | ||||||||||
| 内容記述タイプ | Abstract | |||||||||
| 内容記述 | The renin-angiotensin system (RAS) plays an important role in the regulation of blood pressure, and in the maintenance of electrolyte balance and fluid volume homeostasis. The RAS components include the enzyme renin, its substrate angiotensinogen, and angiotensin converting enzyme (ACE), but the participation of this system in the etiology of human essential hypertension remains unclear. Recently transgenic animals have been instrumental in providing new insights into a variety of cellular processes and biological actions as caused by the introduced genes of interest. In order to assess the functional role of the native human RAS in the development of high blood pressure, we have generated transgenic mice lines harbouring both human renin and human angiotensinogen genes by cross-mating separate lines of transgenic mice carrying either gene. Mice carrying either gene alone did not develop hypertension despite of the observed normal tissue-specific expression of the transgenes. However, strains carrying both genes exhibited a chronically sustained high blood pressure. Administration of a human renin-specific inhibitor (ES-8891) reduced effectively the elevated blood pressure only against the strains carrying both genes, but treatment of an angiotensin converting enzyme inhibitor (Captopril) and a selective antagonist directed at the angiotensin II receptor (DuP 753) reduced blood pressure not only in the dual gene carrier but also in each single gene carriers and wild type mice. These findings indicate that the development of high blood pressure observed in the transgenic mice lines which carry both human renin and angiotensinogen genes was initiated by the interaction between the products of two human genes. | |||||||||
| 言語 | en | |||||||||
| 内容記述 | ||||||||||
| 内容記述タイプ | Other | |||||||||
| 内容記述 | 本文データはCiNiiから複製したものである。 | |||||||||
| 言語 | ja | |||||||||
