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Published on: June 7, 2016
Role of angiotensin II AT1 receptor activation in cardiovascular diseases
Sandrine Billet1, Fréderick Aguilar, Camille Baudry
1Département d'Endocrinologie, Métabolisme et Cancer, Faculté de Médecine Paris Descartes, Institut Cochin, Université Paris Descartes, CNRS UMR8104, Paris, France.
Insights
Angiotensin II (AngII) contributes to cardiovascular fibrosis more than hypertrophy in hypertension. New transgenic mice models reveal AngII
Area of Science:
- Cardiovascular research
- Hypertension mechanisms
- Renal and vascular physiology
Background:
- Angiotensin II (AngII) signaling via AT(1) receptors is implicated in cardiovascular diseases.
- Distinguishing direct AngII effects from hypertension-induced damage is crucial.
- The renin-angiotensin system's role in hypertension-related end-organ damage requires clarification.
Purpose of the Study:
- To investigate the direct role of AngII in cardiovascular damage.
- To differentiate between direct AngII effects and hypertension-induced pathology.
- To elucidate the contribution of AngII to cardiovascular hypertrophy and fibrosis.
Main Methods:
- Development of a novel transgenic mouse model with a constitutively activated AT(1A) receptor.
- Homologous recombination technique for receptor modification.
- Phenotypic analysis including blood pressure, cardiac, renal, and vascular assessments.
Main Results:
- Transgenic mice exhibited moderate hypertension (20 mm Hg) and small kidney artery hypertrophy.
- Cardiac hypertrophy was not observed in these mice.
- A prominent finding was the early and progressive development of cardiovascular fibrosis.
Conclusions:
- Angiotensin II directly promotes cardiovascular fibrosis.
- The renin-angiotensin system plays a minor role in hypertension-induced cardiac hypertrophy.
- Evidence suggests AngII activation significantly contributes to cardiovascular fibrosis in human hypertension.
Abstract:
Numerous clinical studies and experimental investigations using cell culture and animal models suggest that angiotensin II (AngII) via AT(1) receptor activation might induce cardiovascular hypertrophy, fibrosis and atherosclerosis resulting in vascular events such as myocardial infarction, heart failure or stroke and in end-organ damages. However, a question still remains: which part of these damages is due to a direct effect of AngII on its target tissues and which is due to AngII-induced hypertension? In an attempt to answer this question, a new model of transgenic mice, expressing a constitutively activated AT(1A) receptor instead of the wild type receptor has been obtained by homologous recombination. These mice present with a moderate increase of blood pressure (20 mm Hg), hypertrophy of the small kidney arteries but not cardiac hypertrophy. The major phenotypic trait of these mice is the early and progressive development of a cardiovascular fibrosis. In light of these results and those from the literature, there is more and more evidence that in human hypertension, activation of the renin angiotensin system plays a minor role in the development of cardiovascular hypertrophy, but clearly participates to the development of cardiovascular fibrosis.
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