Valsartan Upregulates Kir2.1 in Rats Suffering from Myocardial Infarction via Casein Kinase 2

摘要: Myocardial infarction (MI) results in an increased susceptibility to ventricular arrhythmias, due part decreased inward-rectifier K+ current (IK1), which is mediated primarily by the Kir2.1 protein. The use of renin-angiotensin-aldosterone system antagonists associated with a reduced incidence arrhythmias. Casein kinase 2 (CK2) binds and phosphorylates SP1, transcription factor KCNJ2 that encodes Kir2.1. Whether valsartan represses CK2 activation ameliorate IK1 remodeling following MI remains unclear. Wistar rats suffering from received either or saline for 7 days. protein levels were each detected via Western blot analysis. mRNA examined quantitative real-time PCR. expression was higher at infarct border; accompanied depressed IK1/Kir2.1 level. Additionally, overexpression suppressed KCNJ2/Kir2.1 expression. By contrast, inhibition enhanced expression, establishing regulates Among MI, compared treatment. In vitro, hypoxia inhibited over-expression cells treated abrogated its beneficial effect on KCNJ2/Kir2.1. AT1 receptor antagonist reduces activation, increases thereby ameliorates after rat model.