Reduced abundance of transverse tubules and L-type calcium channels: Another cause of defective contractility in failing ventricular myocytes

Cardiovascular Research

Volumn 49, Issue 2, 2001, Pages 253-256

  Houser, Steven R ^a  

^a TEMPLE UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CALCIUM CHANNEL;

ACTION POTENTIAL; CALCIUM TRANSPORT; CAUSE OF DEATH; CONGESTIVE HEART FAILURE; EXERCISE TOLERANCE; HEART MUSCLE CELL; PRIORITY JOURNAL; PROTEIN STRUCTURE; RECEPTOR BINDING; REVIEW; SARCOPLASMIC RETICULUM; TRANSVERSE TUBULAR SYSTEM;

ANIMALS; CALCIUM; CALCIUM CHANNELS, L-TYPE; CELL MEMBRANE; HEART FAILURE, CONGESTIVE; HUMANS; MYOCARDIAL CONTRACTION; MYOCARDIUM; PROTEINS;

EID: 0035254475     PISSN: 00086363     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0008-6363(00)00305-9     Document Type: Review

References (27)

1. Reduction in density of transverse tubules and L-type Ca channels in canine tachycardia-induced heart failure
2. Excitation-contraction coupling in rat ventricular myocytes after formamide-induced detubulation
3. Calcium current and activation of contraction in ventricular myocardial fibers
4. Contractions induced by a calcium-triggered release of calcium from the sarcoplasmic reticulum of single skinned cardiac cells
5. Reduced contraction and altered frequency response of isolated ventricular myocytes from patients with heart failure
6. Altered myocardial force-frequency relation in human heart failure
7. Alterations in intracellular calcium handling associated with the inverse force-frequency relation in human dilated cardiomyopathy
8. Abnormalities of calcium cycling in the hypertrophied and failing heart
9. Defective excitation-contraction coupling in experimental cardiac hypertrophy and heart failure
10. Quantitative electron microscopic description of heart muscle cells. Application to normal, hypertrophied and thyroxin-stimulated hearts
11. The cellular basis of pacing-induced dilated cardiomyopathy. Myocyte cell loss and myocyte cellular reactive hypertrophy
12. Examination of the transverse tubular system in living cardiac rat myocytes by 2-photon microscopy and digital image-processing techniques
13. Calcium cycling proteins and force-frequency relationship in heart failure
14. Upregulation of Na/Ca exchanger expression and function in an arrhythmogenic rabbit model of heart failure
15. Mechanisms of altered excitation-contraction coupling in canine tachycardia-induced heart failure. I: Experimental studies
16. Alterations of sarcoplasmic reticulum proteins in failing human dilated cardiomyopathy
17. 2+ uptake by cardiac sarcoplasmic reticulum from patients with idiopathic dilated cardiomyopathy
18. Cellular electrophysiology in cardiac hypertrophy and failure
19. Increased availability and open probability of single L-type calcium channels from failing compared with non-failing human ventricle
20. Beta-adrenergic stimulation of calcium channels occurs by potentiation of high-activity gating modes
21. PKA phosphorylation dissociates FKBP12.6 from the calcium release channel (ryanodine receptor): Defective regulation in failing hearts
22. Decreased catecholamine sensitivity and beta-adrenergic-receptor density in failing human hearts
23. Functional consequences of altering myocardial adrenergic receptor signaling
24. Regulation of PKA binding to AKAPs in the heart: Alterations in human heart failure
25. Human heart failure: cAMP stimulation of SR Ca(2+)-ATPase activity and phosphorylation level of phospholamban
26. Reduced Ca(2+)-sensitivity of SERCA 2a in failing human myocardium due to reduced serine-16 phospholamban phosphorylation
27. 2+ sparks in myocytes from infarcted hearts