NDLI: Spironolactone diminishes spontaneous ventricular premature beats by reducing HCN4 protein expression in rats with myocardial infarction.

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Spironolactone diminishes spontaneous ventricular premature beats by reducing HCN4 protein expression in rats with myocardial infarction.

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Spironolactone diminishes spontaneous ventricular premature beats by reducing HCN4 protein expression in rats with myocardial infarction.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Huang, Congxin Yao, Yuan Song, Tao Chen, Yongjun Yang, Jing Li, Haitao Zhang, Jun
Description	Author Affiliation: Song T ( Department of Cardiology, Renmin Hospital of Wuhan University, and Cardiovascular Research Institute,Wuhan University, Wuhan 430060, PR China.)
Abstract	Hyperpolarization-activated current (If) is the major ionic current contributing to the spontaneous diastolic depolarization of cardiac sinus node pacemaker cells. It is mediated by hyperpolarization-activated and cyclic nucleotide-gated (HCN) channels. However, several observations support a potential role of HCN channels in the arrhythmogenesis of working myocardium under pathological conditions. Spironolactone, a classic aldosterone blocker, has been proved to prevent spontaneous ventricular arrhythmias after myocardial infarction (MI). Here, we examined the effect of spironolactone on the expression of HCN channels and ventricular premature beats (VPBs) using a rat MI model. Sprague-Dawley rats were divided into a sham-operated group and MI groups treated with intragastric administration of saline or spironolactone (80 µg/kg/day) for 7 days immediately after ligation of the left coronary artery. Compared to the sham group, HCN2 and HCN4 protein levels were increased in MI rats. Treatment with spironolactone prevented the MI-induced increase of HCN4 protein levels (1.47 ± 0.16 vs. 1.81 ± 0.21, P<0.05). MI rats exhibited a marked increase of VPBs compared to the sham group (104 ± 17 vs. 3 ± 1 VPBs/h, P < 0.05). This the increase was reduced by spironolactone (55 ± 14 vs. 104 ± 17 VPBs/h, P < 0.05). Moreover, If current inhibitor (ivabradine, 0.5 mg/kg) further decreased the occurrence of VPBs in the control and spironolactone groups to the same level (54 ± 13 vs. 49 ± 8 VPBs/h, P > 0.05). In conclusion, spironolactone may prevent ischemia-induced VPBs by reducing HCN4 protein expression to basal levels.
ISSN	17912997
e-ISSN	17913004
Journal	Molecular Medicine Reports
Issue Number	3
Volume Number	4
Language	English
Publisher	Spandidos Publications
Publisher Date	2011-05-01
Publisher Place	Greece
Access Restriction	Open
Subject Keyword	Myocardial Infarction Complications Drug Therapy Potassium Channels Metabolism Spironolactone Therapeutic Use Ventricular Premature Complexes Animals Benzazepines Pharmacology Blotting, Western Heart Rate Drug Effects Hyperpolarization-activated Cyclic Nucleotide-gated Channels Ion Channels Physiopathology Rats, Sprague-dawley Survival Analysis Ultrasonography Research Support, Non-u.s. Gov't Discipline Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology

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