Sarcoplasmic reticulmn Ca2+ release causes myocyte depolarization: Underlying mechanism and threshold for triggered action potentials

Circulation Research

Volumn 87, Issue 9, 2000, Pages 774-780

  Schlotthauer, Klaus ^a   Bers, Donald M ^a  

^a LOYOLA UNIVERSITY MEDICAL CENTER   (United States)

Author keywords

Arrhythmia; Delayed afterdepolarization; Na+ Ca2+ exchanger; Sarcoplasmic reticulum; Transient inward current

Indexed keywords

CAFFEINE; CALCIUM; CATION; CHLORIDE; NIFLUMIC ACID; SODIUM;

ANIMAL CELL; ARTICLE; CALCIUM CURRENT; CALCIUM TRANSPORT; CHLORIDE CURRENT; CONTROLLED STUDY; HEART ARRHYTHMIA; HEART DEPOLARIZATION; HEART MUSCLE POTENTIAL; NONHUMAN; PRIORITY JOURNAL; RABBIT; REGULATORY MECHANISM; SARCOPLASMIC RETICULUM; SODIUM CALCIUM EXCHANGE; ACTION POTENTIAL; ANIMAL; CELL MEMBRANE POTENTIAL; CHEMISTRY; DRUG EFFECT; ELECTROSTIMULATION; HEART MUSCLE; HEART VENTRICLE; METABOLISM; PATCH CLAMP;

ACTION POTENTIALS; ANIMALS; CAFFEINE; CALCIUM; CATIONS; CHLORIDES; ELECTRIC STIMULATION; HEART VENTRICLES; MEMBRANE POTENTIALS; MYOCARDIUM; NIFLUMIC ACID; PATCH-CLAMP TECHNIQUES; RABBITS; SARCOPLASMIC RETICULUM; SODIUM;

EID: 0034721607     PISSN: 00097330     EISSN: None     Source Type: Journal    
DOI: 10.1161/01.RES.87.9.774     Document Type: Article

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