Objective:
Smoking is the major risk factor for cardiovascular diseases. Nicotine is most harmful ingredients in cigarettes. Although there are many reports related on the effects of nicotine on cardiomyocytes, some reports showed nicotine induces cardiomyocyte apoptosis and other reports showed nicotine represses cardiomyocyte hypertrophy. The purpose of this study is to investigate whether nicotine induce/suppress of cardiomyocyte death and hypertrophy.

Methods and Results:
First, we preformed MTT assay to evaluate the toxicity of nicotine in neonatal rat primary cultured cardiomyocytes. Treatment of 1mM nicotine did not damage cardiomyocytes compared to control. Next, cardiomyocytes were treated with nicotine for two hours, after this, stimulated with phenylephrine for 48 hours. Cardiomyocytes were immunostained with α-actinin antibody and measured cell surface area. Nicotine treatment did not induce cardiomyocyte hypertrophy compared to control. Moreover, Nicotine did not suppress phenylephrine-induced cardiomyocyte hypertrophy. Finally, cardiac fibroblasts from neonatal rat heart were pretreated with 1 mM of nicotine for 2 hours and stimulated with TGF-β for 48 hr. Nicotine treatment did not significantly suppressed TGF-β-induced proline intake.

Conclusion:
These results showed that nicotine did not affect directly cardiomyocyte toxicity and hypertrophy. Other compounds in cigarettes may have significant cardiac toxicity.