Abstract: AIM: To explore the effects of pinacidil on the proliferation of rabbit pulmonary arterial smooth muscle cell (PASMC) induced by endothelin-1 in vitro. METHODS: The experimental model of proliferation of rabbit pulmonary arterial smooth muscle cell (PASMC) induced by endothelin-1 in vitro was established and [³H]-thymidine ([³H]-TdR) incorporation and flow cytometric analysis (FCA) were used.RESULTS: Pinacidil markedly inhibited [³H]-TdR incorporation of PASMC induced by ET-1 and held back PASMC from static phase (G₀/G₁) to DNA synthesis (S) and mitotic phase (G₂/M) in the dose-dependent manner.Glibenclimide blocked the effects of pinacidil on [³H]-TdR incorporation. CONCLUSION: Pinacidil has an inhibitive effect on PASMC proliferation induced by ET-1 through activating ATP sensitive potassium (K_ATP) channels and K_ATP channels might play an important pathophysiologic role in the vascular remodeling.Pinacidil is a promising candidate in the treatment of pulmonary hypertension.

Key words: pinacidil, pulmonary arterial smooth muscle cell, endothelin-1, ATP sensitive potassium channels