期刊
CLINICAL SCIENCE
卷 127, 期 9-10, 页码 549-557出版社
PORTLAND PRESS LTD
DOI: 10.1042/CS20130449
关键词
angiotensin-(1-9); angiotensin II; angiotensin type 2 receptor (AT(2)R); cardiovascular damage; renin-angiotensin system
资金
- Fondo Nacional de Desarrollo Cientifico y Tecnologico (FONDECYT) [1100874, 1130550, 1085208]
- Fondo de Fomento al Desarrollo Cientifico y Tecnologico (FONDEF) [D11I1122]
- Comision Nacional de Investigacion Cientifica y Tecnologica (CONICYT) [ACT-1111]
- Fondo de Investigacion Avanzada en Areas Prioritarias (FONDAP) [15130011]
- Millennium Institute of Immunology and Immunotherapy [P09/016-F]
Chronic RAS (renin-angiotensin system) activation by both AngII (angiotensin II) and aldosterone leads to hypertension and perpetuates a cascade of pro-hypertrophic, pro-inflammatory, pro-thrombotic and atherogenic effects associated with cardiovascular damage. In 2000, a new pathway consisting of ACE2 (angiotensin-converting enzyme2), Ang-(1-9) [angiotensin-(1-9)], Ang-(1-7) [angiotensin-(1-7)] and the Mas receptor was discovered. Activation of this novel pathway stimulates vasodilation, anti-hypertrophy and anti-hyperplasia. For some time, studies have focused mainly on ACE2, Ang-(1-7) and the Mas receptor, and their biological properties that counterbalance the ACE/AngII/AT(1)R (angiotensin type 1 receptor) axis. No previous information about Ang-(1-9) suggested that this peptide had biological properties. However, recent data suggest that Ang-(1-9) protects the heart and blood vessels (and possibly the kidney) from adverse cardiovascular remodelling in patients with hypertension and/or heart failure. These beneficial effects are not modified by the Mas receptor antagonist A779 [an Ang-(1-7) receptor blocker], but they are abolished by-the AT(2)R (angiotensin type 2 receptor) antagonist PD123319. Current information suggests that the beneficial effects of Ang-(1-9) are mediated via the AT2R. In the present review, we summarize the biological effects of the novel vasoactive peptide Ang-(1-9), providing new evidence of its cardiovascular-protective activity. We also discuss the potential mechanism by which this peptide prevents and ameliorates the cardiovascular damage induced by RAS activation.
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