Mechanisms that induce the excessive proliferation of vascular wall cells in hypoxic pulmonary hypertension (PH) are not fully understood. Alveolar hypoxia causes sympatho-excitation, and norepinephrine can stimulate |*alpha*_|1-adrenoceptor-dependent hypertrophy/hyperplasia of smooth muscle cells and adventitial fibroblasts. Adrenergic trophic activity is augmented in systemic arteries by injury and altered shear stress, which are key pathogenic stimuli in hypoxic PH, and contributes to neointimal formation and flow-mediated hypertrophic remodeling. Here we examined whether norepinephrine stimulates growth of the pulmonary artery (PA) and if this is augmented in PH. Pulmonary arteries from normoxic and hypoxic rats (9 days of 0.1 FIO₂) were studied in organ culture, where wall tension, PO₂ and PCO₂ were maintained at values present in normal and hypoxic PH rats. Norepinephrine treatment for 72h increased DNA and protein content modestly in normoxic PA (+10%, p < 0.05). In hypoxic PA, these effects were augmented 3 fold (p<0.05) and protein synthesis was increased 34 fold (p<0.05). Inferior thoracic vena cava from normoxic or hypoxic rats was unaffected. Norepinephrine-induced growth in hypoxic PA was dose-dependent, had efficacy endothelin-1, required the presence of wall tension, and was inhibited by _1A-adrenoceptor antagonist. In hypoxic pulmonary vasculature, _1A-adrenoceptor expression was downregulated the least among ₁-AR subtypes. These data demonstrate that norepinephrine has trophic activity in the PA that is augmented by PH. If evident in vivo in the pulmonary vasculature, adrenergic-induced growth may contribute to the vascular hyperplasia that participates in hypoxic pulmonary hypertension.