Angiotensin II type 1a receptor signalling directly contributes to the increased arrhythmogenicity in cardiac hypertrophy

British Journal of Pharmacology

Volumn 170, Issue 7, 2013, Pages 1384-1395

  Yasuno, Shinji ^a   Kuwahara, Koichiro ^a   Kinoshita, Hideyuki ^a   Yamada, Chinatsu ^a   Nakagawa, Yasuaki ^a   Usami, Satoru ^a   Kuwabara, Yoshihiro ^a   Ueshima, Kenji ^a   Harada, Masaki ^a   Nishikimi, Toshio ^a   Nakao, Kazuwa ^a  

^a KYOTO UNIVERSITY   (Japan)

Author keywords

angiotensin; arrhythmia; connexin; hypertrophy

Indexed keywords

ANGIOTENSIN 1A RECEPTOR; CONNEXIN 43; TYROSINE; AGTR1A PROTEIN, MOUSE; ANGIOTENSIN 1 RECEPTOR; ANGIOTENSIN 1 RECEPTOR ANTAGONIST; ANTIARRHYTHMIC AGENT; CACNA1C PROTEIN, MOUSE; CALCIUM CHANNEL L TYPE; GJA1 PROTEIN, MOUSE; MESSENGER RNA; POTASSIUM CHANNEL; SCN5A PROTEIN, MOUSE; SODIUM CHANNEL NAV1.5;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; AORTA CONSTRICTION; ARRHYTHMOGENESIS; ARTICLE; BODY WEIGHT; CONTROLLED STUDY; DISEASE PREDISPOSITION; GENE EXPRESSION; HEART ARRHYTHMIA; HEART CONDUCTION; HEART HYPERTROPHY; HEART LEFT VENTRICLE OVERLOAD; HEART MUSCLE FIBROSIS; HEART VENTRICLE TACHYCARDIA; HEART WEIGHT; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN PHOSPHORYLATION; TISSUE LEVEL; ANIMAL; C57BL MOUSE; CARDIOMEGALY; DEFICIENCY; DISEASE MODEL; DRUG EFFECTS; GENE EXPRESSION REGULATION; GENETICS; GENOTYPE; KNOCKOUT MOUSE; METABOLISM; PATHOPHYSIOLOGY; PHENOTYPE; PHOSPHORYLATION; SIGNAL TRANSDUCTION; TACHYCARDIA, VENTRICULAR;

ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS; ANIMALS; ANTI-ARRHYTHMIA AGENTS; CALCIUM CHANNELS, L-TYPE; CARDIOMEGALY; CONNEXIN 43; DISEASE MODELS, ANIMAL; GENE EXPRESSION REGULATION; GENOTYPE; MICE; MICE, INBRED C57BL; MICE, KNOCKOUT; NAV1.5 VOLTAGE-GATED SODIUM CHANNEL; PHENOTYPE; PHOSPHORYLATION; POTASSIUM CHANNELS; RECEPTOR, ANGIOTENSIN, TYPE 1; RNA, MESSENGER; SIGNAL TRANSDUCTION; TACHYCARDIA, VENTRICULAR;

EID: 84887728205     PISSN: 00071188     EISSN: 14765381     Source Type: Journal    
DOI: 10.1111/bph.12328     Document Type: Article

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