Modulation of Ca2+ release in cardiac myocytes by changes in repolarization rate: Role of phase-1 action potential repolarization in excitation-contraction coupling

Circulation Research

Volumn 90, Issue 2, 2002, Pages 165-173

  Sah, Rajan ^a,b   Ramirez, Rafael J ^a,b   Backx, Peter H ^a,b,c  

^a HEART AND STROKE FOUNDATION OF CANADA   (Canada)

^b UNIVERSITY HEALTH NETWORK   (Canada)

^c TORONTO GENERAL HOSPITAL   (Canada)

Author keywords

Calcium sparks; Confocal microscopy; Electrophysiology; Heart disease

Indexed keywords

CALCIUM CHANNEL L TYPE; ISOPRENALINE;

ACTION POTENTIAL; ARTICLE; BETA ADRENERGIC STIMULATION; CALCIUM CURRENT; CALCIUM TRANSPORT; CELL ISOLATION; CONFOCAL MICROSCOPY; EXCITATION CONTRACTION COUPLING; HEART MUSCLE CELL; HEART REPOLARIZATION; POTASSIUM CURRENT; PRIORITY JOURNAL; SIGNAL TRANSDUCTION; TRANSPORT KINETICS;

ACTION POTENTIALS; ADRENERGIC BETA-AGONISTS; ANIMALS; CALCIUM; CALCIUM CHANNELS, L-TYPE; CALCIUM SIGNALING; CELL SEPARATION; COMPUTER SIMULATION; ELECTRIC STIMULATION; HUMANS; ISOPROTERENOL; MICROSCOPY, CONFOCAL; MODELS, CARDIOVASCULAR; MYOCARDIAL CONTRACTION; MYOCARDIUM; PATCH-CLAMP TECHNIQUES; RABBITS; RATS; REACTION TIME; SARCOPLASMIC RETICULUM;

EID: 0037040162     PISSN: 00097330     EISSN: None     Source Type: Journal    
DOI: 10.1161/hh0202.103315     Document Type: Article

References (31)

1. Mechanisms of altered excitation-contraction coupling in canine tachycardia-induced heart failure, I: Experimental studies
2. 2+ sparks in myocytes from infarcted hearts
3. Defective excitation contraction coupling in experimental cardiac hypertrophy and heart failure
4. Intracellular calcium handling in isolated ventricular myocytes from patients with terminal heart failure
5. Decreased sarcoplasmic reticulum calcium content is responsible for defective excitation-contraction coupling in canine heart failure
6. + currents in isolated human ventricular myocytes from patients with terminal heart failure
7. Ionic mechanism of action potential prolongation in ventricular myocytes from dogs with pacing-induced heart failure
8. i in rat ventricular myocytes following myocardial infarction
9. The roles of ion channels in an inherited heart disease: Molecular genetics of the long QT syndrome
10. Ionic mechanisms for prolongation of refractoriness and their proarrhythmic and antiarrhythmic correlates
11. |o| in shaping action potential morphology and duration
12. Effects of action potential duration on excitation-contraction coupling in rat ventricular myocytes: Action potential voltage-clamp measurements
13. Alterations in action potential profile enhance excitation-contraction coupling in rat cardiac myocytes
14. 2+ exchange in the infarcted heart: Implications for excitation-contraction coupling
15. 2+ spikes" in rat cardiac myocytes
16. 2+ release during excitation-contraction coupling in cardiac myocytes
17. Chloride channel inhibition blocks the protection of ischemic preconditioning and hypo-osmotic stress in rabbit ventricular myocardium
18. 2+ release sites in rat cardiac myocytes
19. 2+ sparks and local control theories for cardiac excitation-contraction coupling
20. |o| in myocytes isolated from the human right ventricle
21. Simulation study of cellular electric properties in heart failure
22. 2+ channels of cardiac myocytes
23. 2+ exchanger in mammalian cardiac myocytes
24. 2+ reuptake in rat ventricular myocytes
25. 2+ transient in rat myocytes during β-adrenergic stimulation
26. 2+ release cascade by β-adrenergic stimulation in rat ventricular myocytes
27. Potassium channel down-regulation in heart failure
28. + current on the guinea pig action potential
29. Molecular dissection of cardiac repolarization by in vivo Kv4.3 gene transfer
30. Altered β-adrenergic receptor gene regulation and signaling in chronic heart failure