2-B-P-005 〇喜多 紗斗美^1,2、前田 結菜¹、谷 和佳奈¹、根本 隆行²、喜多 知²、岩本 隆宏² Satomi Kita^1,2, Yuina Maeda¹, Wakana Tani¹, Takayuki Nemoto², Tomo Kita², Takahiro Iwamoto^{2 1}徳島文理大・薬・薬理、²福岡大・医・薬理 ¹Dept Pharmacol, Facul Phrarmaceut Sci, Tokushima Bunri Univ, ²Dept Pharmacol, Facul Med, Fukuoka Univ Pulmonary arterial hypertension (PAH) is a severe and progressive disease that leads to right heart failure. The pathogenesis of PAH is generally characterized by vasoconstriction, upregulated proliferation, migration, and pulmonary vascular remodeling in lung tissue. Recent studies using genetic analyses and experimental models have suggested that the hypercontraction of pulmonary arteries induced by Ca²⁺ signaling abnormality may be involved in the pathogenesis of PAH. We recently showed that the upregulation of mitochondrial Na⁺/Ca²⁺ exchanger (NCLX) contributes to the development of hypoxia-induced PAH, using NCLX genetically engineered mice. In the present study, we investigated the pathological mechanisms of NCLX in hypoxia-induced pulmonary hypertension. Pressure-induced arterial constriction was relaxed by specific NCLX inhibitor CGP-37157. Moreover, CGP-37157 suppressed hypoxia-induced migration of pulmonary arterial smooth muscle cells. These findings suggest that NCLX contributes to the development of pulmonary hypertension by promoting vascular hypercontraction and migration of pulmonary artery cells.