Effect of ATP-Sensitive Potassium Channel Agonists on Ventricular Remodeling in Healed Rat Infarcts

Effect of ATP-Sensitive Potassium Channel Agonists on Ventricular Remodeling in Healed Rat Infarcts Tsung-Ming Lee, Mei-Shu Lin, Nen-Chung Chang To assess whether ATP-sensitive potassium channel (KATP ) agonists are effective in improving ventricular remodeling, infarcted rats were randomly assigned...

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Bibliographic Details
Published in:Journal of the American College of Cardiology 2008-04, Vol.51 (13), p.1309-1318
Main Authors: Lee, Tsung-Ming, MD, FESC, Lin, Mei-Shu, PhD, Chang, Nen-Chung, MD, PhD, FACC
Format: Article
Language:English
Subjects:
Adenosine triphosphatase
Animals
Biological and medical sciences
Cardiology
Cardiology. Vascular system
Cardiovascular
Drug dosages
Glucose
Glyburide - pharmacology
Heart attacks
Hemodynamics
Hypertrophy, Left Ventricular - physiopathology
Immunohistochemistry
Internal Medicine
KATP Channels - agonists
Kinases
Laboratory animals
Male
Medical sciences
Muscle Cells
Myocardial Infarction - physiopathology
Nicorandil - pharmacology
Phosphorylation
Pinacidil - pharmacology
Potassium
Rats
Rats, Wistar
Risk Factors
Rodents
Standard deviation
Time Factors
Ventricular Remodeling
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Summary:Effect of ATP-Sensitive Potassium Channel Agonists on Ventricular Remodeling in Healed Rat Infarcts Tsung-Ming Lee, Mei-Shu Lin, Nen-Chung Chang To assess whether ATP-sensitive potassium channel (KATP ) agonists are effective in improving ventricular remodeling, infarcted rats were randomly assigned to receive either vehicle, nicorandil, pinacidil, glibenclamide, or a combination of nicorandil and glibenclamide or pinacidil and glibenclamide. In the vehicle, increased synthesis of p70S6 kinase messenger ribonucleic acid was confirmed by reverse transcription-polymerase chain reaction consistent with the results of immunohistochemistry and Western blot for phosphorylated p70S6 kinase. Compared with vehicle, KATP channel agonist-treated rats showed significantly attenuated cardiomyocyte hypertrophy, which was abolished by administering glibenclamide. Thus, activation of KATP channels can attenuate ventricular remodeling probably through a S6 kinase-dependent pathway after infarction.
ISSN:0735-1097
1558-3597
DOI:10.1016/j.jacc.2007.11.067