Transient outward potassium channel regulation in healthy and diabetic hearts

Diabetic patients have a higher incidence of cardiac arrhythmias, including ventricular fibrillation and sudden death, and show important alterations in the electrocardiogram, most of these related to the repolarization. In myocytes isolated from diabetic hearts, the transient outward K+ current (It...

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Bibliographic Details
Published in:Canadian journal of physiology and pharmacology 2009-02, Vol.87 (2), p.77-83
Main Authors: GALLEGO, Mónica, ALDAY, Aintzane, URRUTIA, Janire, CASIS, Oscar
Format: Article
Language:English
Subjects:
Action Potentials
Animals
Arrhythmias, Cardiac - metabolism
Arrhythmias, Cardiac - physiopathology
Biological and medical sciences
Cardiology
Cardiovascular disease
Diabetes
Diabetes Complications - metabolism
Diabetes Complications - physiopathology
Diabetics
Fundamental and applied biological sciences. Psychology
Health aspects
Heart diseases
Humans
Insulin
Kinetics
Kv1.4 Potassium Channel - metabolism
Myocytes, Cardiac - metabolism
Physiological aspects
Potassium
Potassium channels
Potassium Channels - metabolism
Risk factors
Shal Potassium Channels - metabolism
Sympathetic Nervous System - physiopathology
Type 1 diabetes
Vertebrates: anatomy and physiology, studies on body, several organs or systems
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Summary:Diabetic patients have a higher incidence of cardiac arrhythmias, including ventricular fibrillation and sudden death, and show important alterations in the electrocardiogram, most of these related to the repolarization. In myocytes isolated from diabetic hearts, the transient outward K+ current (Ito) is the repolarizing current that is mainly affected. Type 1 diabetes alters Ito at 3 levels: the recovery of inactivation, the responsiveness to physiologic regulators, and the functional expression of the channel. Diabetes slows down Ito recovery of inactivation because it triggers the switching from fast-recovering Kv4.x channels to the slow-recovering Kv1.4. Diabetic animals also have decreased responsiveness of Ito towards the sympathetic nervous system; thus, the diabetic heart develops a resistance to its physiologic regulator. Finally, diabetes impairs support of various trophic factors required for the functional expression of the channel and reduces Ito amplitude by decreasing the amount of Kv4.2 and Kv4.3 proteins.
ISSN:0008-4212
1205-7541
DOI:10.1139/Y08-106