AT2, judgment day: Which angiotensin receptor is the culprit in cardiac hypertrophy?

Circulation

Volumn 104, Issue 3, 2001, Pages 247-248

  Schneider, Michael D ^a   Lorell, Beverly H ^b  

^a BAYLOR COLLEGE OF MEDICINE   (United States)

^b HARVARD MEDICAL SCHOOL   (United States)

Author keywords

Angiotensin; Cardiac hypertrophy; Editorials; Gene targeting; Mice; Receptor

Indexed keywords

ANGIOTENSIN RECEPTOR; DIPEPTIDYL CARBOXYPEPTIDASE INHIBITOR; GROWTH FACTOR; MITOGEN ACTIVATED PROTEIN KINASE;

EDITORIAL; GENE DELETION; HEART FAILURE; HEART MUSCLE CELL; HEART MUSCLE FIBROSIS; HEART VENTRICLE HYPERTROPHY; LONG TERM CARE; PRIORITY JOURNAL; SYSTOLIC BLOOD PRESSURE; TRANSDUCER; VASOCONSTRICTION;

EID: 0035902610     PISSN: 00097322     EISSN: None     Source Type: Journal    
DOI: 10.1161/01.CIR.104.3.247     Document Type: Editorial

References (20)

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13. Effects on blood pressure and exploratory behavior of mice lacking angiotensin II type-2 receptor
14. Angiotensin II type 2 receptor overexpression activates the vascular kinin system and causes vasodilation
15. 2 receptors differentially regulate angiopoietin-2 and vascular endothelial growth factor expression and angiogenesis by modulating heparin binding-epidermal growth factor (EGF)-mediated EGF receptor transactivation
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19. Angiotensin type 2 receptor dephosphorylates Bcl-2 by activating mitogen-activated protein kinase phosphatase-1 and induces apoptosis
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