Abstract
Nicorandil, the first clinically applied ATP-sensitive K+ channel (K+ATP) opener with nitrate property, has demonstrated cardioprotective effects in patients with multiples of heart diseases. However, it is unknown whether nicorandil has effects on left ventricular (LV) remodeling in rats with ischemic heart failure and the potential mechanisms remain unclear. In this study, we investigated the effects of nicorandil on cardiac function, LV remodeling, and Bax expression in myocardium of LV in rats with ischemic heart failure. We found that nicorandil could improve not only the general condition, but also the cardiac function in rats with ischemic heart failure. The data also demonstrated that nicorandil reduced the hypertrophy and fibrosis of LV in rats with ischemic heart failure. Furthermore, nicorandil suppressed the protein level of Bax expression in LV myocardium. Taken together, these results suggest that nicorandil exerts its cardioprotective effect and improves LV remodeling in rats with ischemic heart failure. The mechanism might be relative to the inhibitory effect of nicorandil on the protein level of Bax expression in LV myocardium.
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