Panx1 deficiency does not protect from chronic hypoxic pulmonary hypertension. Mice with a tamoxifen-induced deletion of Panx1 in smooth muscle cells (SMMHC-CreERT2/Panx1^fl/fl) or endothelial cells (Cdh5-CreERT2/Panx1^fl/fl) or corresponding wild-type controls (C57BL/6J) were kept under normoxic (21% O₂) or hypoxic (10% O₂) conditions for weeks for induction of chronic hypoxic pulmonary hypertension. As compared to normoxia (white bars), hypoxia (grey bars) caused (A) an increase in right ventricular systolic pressure (RVSP) as well as (B) right ventricular hypertrophy [right ventricular weight/(left ventricular + septal weight); Fulton index] in C57BL/6J mice. Similar effects were observed in Cdh5-CreERT2/Panx1^fl/fl and SMMHC-CreERT2/Panx1^fl/fl mice with no significant differences between genotypes except for Fulton index which was lower in Cdh5-CreERT2/Panx1^fl/fl as compared to C57BL/6J mice. (C) Representative haematoxylin and eosin stainings show lung vascular remodelling in chronic hypoxic mice. Black arrows highlight pulmonary arterioles of 25–50 µm diameter. Wall thickness was determined at four different locations and mean wall thickness was normalized to the shortest cross-sectional diameter. (D) Medial thickening in pulmonary arterioles, was observed in C57BL/6J, Cdh5-CreERT2/Panx1^fl/fl, and SMMHC-CreERT2/Panx1^fl/fl mice as characteristics of pulmonary hypertension (n = 8–10 per group). Data are mean ± SEM; data were analysed using one-way ANOVA; *P < 0.05.