2-B-P-056 〇安田 純平、松村 早季子、納富 拓也、陳 以珊、西谷（中村） 友重 Jumpei Yasuda, Sakiko Matsumura, Takuya Notomi, I-Shan Chen, Tomoe Y. Nakamura-Nishitani 和歌山県立医科大・医・薬理学講座 Dept. Pharmacol., Sch. Med., Wakayama Medical Univ. Smoking is well known as a major risk factor of cardiovascular diseases. However, the direct effects of smoking substances on cardiomyocyte and its cellular mechanism have not been fully clarified. In this study, we examined the effects of CSE on the contractile function, intracellular Ca²⁺ dynamics, and mitochondrial function using cultured or freshly isolated rat ventricular myocytes and human iPS-derived cardiomyocytes. CSE at concentration above 0.1% decreased the spontaneous beating rate of cultured rat cardiomyocytes in a time- and concentration-dependent manner. 1% CSE reduced the cell shortening of freshly isolated cardiomyocytes. Similar contractile dysfunctions were also observed in human iPS-derived cardiomyocytes. In contrast, 1% CSE increased intracellular Ca²⁺ transient amplitude, often triggered spike-shaped Ca²⁺ transients. Kinetic analysis indicated that CSE enhanced Ca²⁺ uptake into the SR. These results suggest that abnormal Ca²⁺ entry/release in the SR occurred upon CSE treatment. Furthermore, CSE induced a decrease in mitochondrial membrane potential, an early event in cellular damage that can be caused by abnormal intracellular Ca²⁺ dynamics. Taken together, these results demonstrate that CSE weakens contractile function of cardiomyocytes via abnormal Ca²⁺-medicated dysregulation of mitochondrial function.