Cardiac-specific overexpression of the human type 1 angiotensin II receptor causes delayed repolarization

Cardiovascular Research

Volumn 78, Issue 1, 2008, Pages 53-62

  Rivard, Katy ^a,b   Paradis, Pierre ^c,d   Nemer, Mona ^c   Fiset, Céline ^a,b  

^a MONTREAL HEART INSTITUTE   (Canada)

^b UNIVERSITÉ DE MONTRÉAL   (Canada)

^c CLIN RESEARCH INSTITUTE OF MONTREAL   (Canada)

^d MCGILL UNIVERSITY   (Canada)

Author keywords

Angiotensin II; Arrhythmias; K+ currents; Transgenic mice; Ventricular repolarization

Indexed keywords

ANGIOTENSIN 2 RECEPTOR; INWARDLY RECTIFYING POTASSIUM CHANNEL;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CALCIUM TRANSPORT; CONTROLLED STUDY; GENE OVEREXPRESSION; HEART ARRHYTHMIA; HEART REPOLARIZATION; HEART VENTRICLE ARRHYTHMIA; HEART VENTRICLE REMODELING; INCIDENCE; MALE; MOUSE; NONHUMAN; POTASSIUM CURRENT; PRIORITY JOURNAL; PROTEIN ANALYSIS; QT PROLONGATION; RISK FACTOR; SUDDEN DEATH;

ACTION POTENTIALS; AGE FACTORS; ANIMALS; ARRHYTHMIAS, CARDIAC; DELAYED RECTIFIER POTASSIUM CHANNELS; ELECTROCARDIOGRAPHY; HEART CONDUCTION SYSTEM; HEART VENTRICLES; HUMANS; LONG QT SYNDROME; MALE; MICE; MICE, INBRED C57BL; MICE, TRANSGENIC; MYOCARDIUM; POTASSIUM; RECEPTOR, ANGIOTENSIN, TYPE 1; TIME FACTORS; UP-REGULATION; VENTRICULAR REMODELING;

EID: 41149107344     PISSN: 00086363     EISSN: 17553245     Source Type: Journal    
DOI: 10.1093/cvr/cvn020     Document Type: Article

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