renin

出典: meddic

レニン

WordNet   license wordnet

「a proteolytic enzyme secreted by the kidneys; catalyzes the formation of angiotensin and thus affects blood pressure」

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2016/10/24 22:59:52」(JST)

wiki en

[Wiki en表示]

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

英文文献

  • Effects of a domain-selective ACE inhibitor in a mouse model of chronic angiotensin II-dependent hypertension.
  • Burger D1, Reudelhuber TL2, Mahajan A3, Chibale K3, Sturrock ED4, Touyz RM.Author information 1*Kidney Research Centre, Ottawa Hospital Research Institute, University of Ottawa, Ottawa, Canada.2†Clinical Research Institute of Montreal, Montreal, Canada.3‡Department of Chemistry and South African Medical Research Council Drug Discovery and Development Research Unit, University of Cape Town, Rondebosch, South Africa.4§Institute of Infectious Diseases and Molecular Medicine and Division of Medical Biochemistry, University of Cape Town, Cape Town, South Africa.AbstractThe somatic isozyme of ACE (angiotensin I-converting enzyme) comprises two distinct zinc-dependent catalytic domains with different substrate specificities for angiotensin I (cleaved selectively by the C-domain) and bradykinin (cleaved equally efficiently by both the N- and C-domains). Classical ACEIs (ACE inhibitors) target both domains, with side effects such as cough and angio-oedema being attributed, in part, to N-domain inhibition, probably through bradykinin accumulation. We questioned whether a novel C-domain-selective ACEI (lisW-S) has anti-hypertensive effects without influencing bradykinin status. AngII (angiotensin II)-dependent hypertension was studied in mice that express active human renin in the liver (TtRhRen). Compared with wild-type littermates, TtRhRen mice displayed cardiac hypertrophy and had significantly elevated SBP [systolic BP (blood pressure)] as determined by tail cuff sphygmomanometry (150±3 compared with 112±5 mmHg; P<0.05) and telemetry (163±3 compared with 112±2 mmHg; P<0.01). Treatment with the non-selective ACEI lisinopril (1 mg/kg of body weight per day via an osmotic mini-pump for 2 weeks) reduced SBP (127±3 compared with. 154±6; P<0.05). Similarly, treatment with the C-domain selective ACEI lisW-S (lisinopril-tryptophan; 3.6 mg/kg of body weight per day via an osmotic mini-pump for 2 weeks) reduced BP. Treatment with lisinopril or lisW-S significantly reduced levels of AngII in kidneys (~4-fold; P<0.001). Ang-(2-8) [angiotensin-2-8)] was significantly reduced by lisinopril, but not by lisW-S. Plasma bradykinin levels were significantly increased only in the lisinopril group. These data suggest that C-domain-selective ACEIs reduce BP and AngII levels similarly to classical ACEIs. C-domain-selective ACEIs have the potential to avoid undesirable effects on the bradykinin system common to classic ACEIs and may represent a novel approach to the treatment of hypertension.
  • Clinical science (London, England : 1979).Clin Sci (Lond).2014 Jul 1;127(1):57-63. doi: 10.1042/CS20130808.
  • The somatic isozyme of ACE (angiotensin I-converting enzyme) comprises two distinct zinc-dependent catalytic domains with different substrate specificities for angiotensin I (cleaved selectively by the C-domain) and bradykinin (cleaved equally efficiently by both the N- and C-domains). Classical ACE
  • PMID 24506807
  • Angiotensin-(1-7) and angiotensin-(1-9): function in cardiac and vascular remodelling.
  • McKinney CA1, Fattah C1, Loughrey CM1, Milligan G2, Nicklin SA1.Author information 1*Institute of Cardiovascular and Medical Sciences, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, U.K.2†Institute of Molecular Cell and Systems Biology, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, U.K.AbstractThe RAS (renin-angiotensin system) is integral to cardiovascular physiology; however, dysregulation of this system largely contributes to the pathophysiology of CVD (cardiovascular disease). It is well established that AngII (angiotensin II), the main effector of the RAS, engages the AT1R (angiotensin type 1 receptor) and promotes cell growth, proliferation, migration and oxidative stress, all processes which contribute to remodelling of the heart and vasculature, ultimately leading to the development and progression of various CVDs, including heart failure and atherosclerosis. The counter-regulatory axis of the RAS, which is centred on the actions of ACE2 (angiotensin-converting enzyme 2) and the resultant production of Ang-(1-7) [angiotensin-(1-7)] from AngII, antagonizes the actions of AngII via the receptor Mas, thereby providing a protective role in CVD. More recently, another ACE2 metabolite, Ang-(1-9) [angiotensin-(1-9)], has been reported to be a biologically active peptide within the counter-regulatory axis of the RAS. The present review will discuss the role of the counter-regulatory RAS peptides Ang-(1-7) and Ang-(1-9) in the cardiovascular system, with a focus on their effects in remodelling of the heart and vasculature.
  • Clinical science (London, England : 1979).Clin Sci (Lond).2014 Jun 1;126(12):815-27. doi: 10.1042/CS20130436.
  • The RAS (renin-angiotensin system) is integral to cardiovascular physiology; however, dysregulation of this system largely contributes to the pathophysiology of CVD (cardiovascular disease). It is well established that AngII (angiotensin II), the main effector of the RAS, engages the AT1R (angiotens
  • PMID 24593683
  • The central renin-angiotensin system and sympathetic nerve activity in chronic heart failure.
  • Zucker IH, Xiao L, Haack KK.Author information *Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198, U.S.A.AbstractCHF (chronic heart failure) is a multifactorial disease process that is characterized by overactivation of the RAAS (renin-angiotensin-aldosterone system) and the sympathetic nervous system. Both of these systems are chronically activated in CHF. The RAAS consists of an excitatory arm involving AngII (angiotensin II), ACE (angiotensin-converting enzyme) and the AT1R (AngII type 1 receptor). The RAAS also consists of a protective arm consisting of Ang-(1-7) [angiotensin-(1-7)], the AT2R (AngII type 2 receptor), ACE2 and the Mas receptor. Sympatho-excitation in CHF is driven, in large part, by an imbalance of these two arms, with an increase in the AngII/AT1R/ACE arm and a decrease in the AT2R/ACE2 arm. This imbalance is manifested in cardiovascular-control regions of the brain such as the rostral ventrolateral medulla and paraventricular nucleus in the hypothalamus. The present review focuses on the current literature that describes the components of these two arms of the RAAS and their imbalance in the CHF state. Moreover, the present review provides additional evidence for the relevance of ACE2 and Ang-(1-7) as key players in the regulation of central sympathetic outflow in CHF. Finally, we also examine the effects of exercise training as a therapeutic strategy and the molecular mechanisms at play in CHF, in part, because of the ability of exercise training to restore the balance of the RAAS axis and sympathetic outflow.
  • Clinical science (London, England : 1979).Clin Sci (Lond).2014 May;126(10):695-706. doi: 10.1042/CS20130294.
  • CHF (chronic heart failure) is a multifactorial disease process that is characterized by overactivation of the RAAS (renin-angiotensin-aldosterone system) and the sympathetic nervous system. Both of these systems are chronically activated in CHF. The RAAS consists of an excitatory arm involving AngI
  • PMID 24490814

和文文献

  • レニン-アンジオテンシン-アルドステロン系を阻害する薬物 : ACE阻害薬とAT₁受容体拮抗薬の特徴
  • 心腎連関における交感神経系の関与 (特集 循環器疾患と交感神経系)
  • Atp6ap2/(プロ)レニン受容体の網膜発生期における細胞極性への関与 (平成26年度日本眼科学会学術奨励賞 受賞論文総説)

関連リンク

Enzyme secreted by the kidney (and also, possibly, by the placenta) that is part of a physiological system that regulates blood pressure. In the blood, renin acts on a protein...
An over-active renin-angiotension system leads to vasoconstriction and retention of sodium and water. These effects lead to hypertension. Therefore, renin inhibitors can be used for the treatment of hypertension. [18] [19] This is ...

関連画像

renin angiotensin aldosterone reflex renin systemReninSơ đồ hệ renin-angiotensin 19946/Renin-angiotensin-system-pic.jpg the renin angiotensin aldosterone system


★リンクテーブル★
リンク元レニン」「prorenin
拡張検索renin-angiotensin-aldosterone system」「renin-angiotensin」「N-formylkynurenine」「formylkynurenine

レニン」

  [★]

renin
アンジオテンシノゲンアンジオテンシン

分類

産生組織

標的組織

作用

分泌の調整 (PT. 480)

  • 1. 交感神経刺激
循環中枢からの刺激→レニン放出↑ β1受容体を介する
立位 → 交感神経亢進(おそらく脳への血行を保つため) → レニン放出↑
  • 2. 腎動脈圧
腎動脈圧↓→レニン放出↑
腎動脈圧↑→レニン放出↓
腎臓の輸入細動脈の圧受容器による
cf.腎動脈動脈狭窄により血流↓→レニンアンジオテンシンアルドステロン系↑→血圧↑
  • 3. 遠位尿細管濾液中のNaCl濃度↓
遠位尿細管濾液中のNaCl濃度↓→レニン放出↑
緻密斑細胞により検出される
血漿濃度や輸入細動脈圧の減少はGFRを減少させ、それによって遠位尿細管濾液中のNaCl濃度を減少させる
  • 4. アンジオテンシンII
  • ネガティブフィードバック制御を受ける。
  • アンジオテンシンII↑→レニン↓

分子機構

臨床関連


prorenin」

  [★]

プロレニン

renin


renin-angiotensin-aldosterone system」

  [★] レニン-アンギオテンシン-アルドステロン系 RAAS

renin-angiotensin」

  [★] レニン-アンギオテンシン

N-formylkynurenine」

  [★] N-ホルミルキヌレニン

formylkynurenine」

  [★] ホルミルキヌレニン


"http://meddic.jp/renin" より作成


★コメント★

[メモ入力エリア]
※コメント5000文字まで
ニックネーム:
コメント:




表示
個人用ツール


  meddic.jp

リンク
連絡