Changes in Ca2+ cycling proteins underlie cardiac action potential prolongation in a pressure-overloaded guinea pig model with cardiac hypertrophy and failure

Circulation Research

Volumn 86, Issue 5, 2000, Pages 558-570

  Ahmmed, Gias U ^c   Dong, Pei Hong ^c   Song, Guoji ^c   Ball, Nancy A ^c   Xu, Yanfang ^c   Walsh, Richard A ^a   Chiamvimonvat, Nipavan ^b  

^a CASE WESTERN RESERVE UNIVERSITY SCHOOL OF MEDICINE   (United States)

^b UNIVERSITY OF CINCINNATI COLLEGE OF MEDICINE   (United States)

^c NONE

Author keywords

Action potential; Ca2+ current; Cardiac failure; Cardiac hypertrophy; Guinea pig

Indexed keywords

ADENOSINE TRIPHOSPHATASE (CALCIUM); CALCIUM; POTASSIUM; SODIUM;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CALCIUM CURRENT; CONTROLLED STUDY; GUINEA PIG; HEART FAILURE; HEART HYPERTROPHY; HEART MUSCLE POTENTIAL; HEART REPOLARIZATION; HEART VENTRICLE OVERLOAD; MALE; NONHUMAN; POTASSIUM CURRENT; PRIORITY JOURNAL; SARCOPLASMIC RETICULUM; SODIUM CALCIUM EXCHANGE; SODIUM CURRENT;

EID: 0343674495     PISSN: 00097330     EISSN: None     Source Type: Journal    
DOI: 10.1161/01.RES.86.5.558     Document Type: Article

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