文档介绍：
Effects of propranolol on transient outward potassium
channel in infarcted rat heart#
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XU Chaoqian, LIANG Haihai, GUAN Xiaoxiang, SHAN Hongli*
(Department of Pharmacology,Harbin Medical University,Harbin,150086)
Abstract: Previous studies have proved that reductions in repolarizing currents occur in post-infracted
myocytes and contribute to various arrhythmias, especially, life-threatening ventricular arrhythmia. In
this paper we studied whether propranolol could restore action potential duration (APD), transient
outward potassium current (Ito), and its gene expression in myocardium of rats after myocardial
infarction (MI). Our findings showed that arrhythmias were induced in MI group. Patch clamp studies
revealed that APD was prolonged and Ito was reduced significantly from ± pA/pF in control
group to ± pA/pF in MI group (p<). Meanwhile, protein was up-regulated after
myocardial infarction and restored with propranolol treatment. Our results also showed that PKA was
decreased after propranolol treatment, indicating that the phosphorylation of expression by PKA
was decreased, which contributes to the recovery of Ito and APD. That may be the possible reason why
propranolol reduced the incidence of arrhythmias.
Key words: Ito, , PKA, propranolol
0 Introduction
Life-threatening ventricular arrhythmia which is secondary to myocardial infarction is
a predictor of sudden cardiac death. Cardiac muscle cells experience ventricular
remodeling after infarction [1, 2], and this process involves in myocytes hypertrophy
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and gene expression alteration in surviving cardiomyocytes
[3, 4, 5]
remodeling process is action potential (AP) prolongation[6,7,8], which itself is
arrhythmogenic [9]. The AP prolongation has been associated with transient outward
potassium current (Ito) down-regulation and its channel expression change in
post-infracted myocardial cells [8, 10].
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In cardiac myocytes, I