| Background:It is known that about half of patients with congest heart failure (CHF)died due to sudden cardiac death induced by malignancy ventricular arrhythmia. Itwas related closely to the electrophysiological characteristic of ventricular cellsduring heart failure. The heart inevitably suffers increasing ventricular load duringheart failure which leads to ventricular remodeling. Ventricular remodeling is anessential element to heart failure which including electrical remodeling, structureremodeling, and function remodeling. Ion channel remodeling of ventricular cells isthe pivotal of electrical remodeling, it contributed to the high incidence of malignancyventricular arrhythmia in heart failure patients. Previously studies showed that theactivation of angiotensin II receptor I type (AT1) contributed to ventricular remoldingstimulated by mechanical stretch, and the inhibition of renin-angiotensin system (RAS)was effective to the prevention and treatment of ventricular arrhythmia induced byheart failure.Objective:To explore the change of delayed rectifier potassium channel expressionof ventricular myocytes in heart failure rats, and the regulation effects of AT1signalin the change.Methods:The heart failure model of Sprague Dawley (SD) rats was established byabdominal aorta banding operation. Forty SD rats were randomly divided into fourgroups according to the different intervention for eight weeks: control group (shamoperation), heart failure (HF) group (abdominal aorta banding), telmisartan (Tel,3.57mg.kg-1.d-1) group (sham operation plus Tel treatment) and HF+Tel group(abdominal aorta banding plus Tel treatment). Left ventricular ejection fraction (LVEF)and left ventricular posterior wall thickness (LVPWd) were measured by ultrasoniccardiogram before and after intervention. NT-proBNP concentration in serum wasmeasured by enzyme-linked immuno sorbent assay. The mRNA and protein expression of delayed rectifier potassium channel (KCNH2,KCNQ1,KCNE1, KCNE2)were detected by Western-Blot and real-time reverse transcriptase-polymerase chainreaction (real-time RT-PCR) analysis.Results:Abdominal aorta banding increased the NT-proBNP concentration in rats’serum and promoted LVPWd, which indicating ventricular remodeling and heartfailure. The mRNA expression of KCNH2and KCNQ1were significantly increasedin rats of HF group, whereas KCNE1and KCNE2markedly decreased, and theprotein expression of KCNH2and KCNQ1were obviously decreased. Telmisartanprevented heart failure-induced alterations in the above mentioned genes and proteinsexpression, NT-proBNP concentration, and LVPWd.Conclusions:Temisartan intervention significantly inhibited the expressionalterations of delay rectification potassium channel genes and proteins in ventricularmyocytes of heart failure rats, it indicated that AT1signal plays a regular role in thechannel remodeling. |
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