Bronchopulmonary dysplasia (BPD) and emphysema are significant global health problems at the extreme stages of life. Both are characterized by alveolar simplification and abnormal distal airspace enlargement due to arrested development or loss of alveoli, respectively. Both lack effective treatments. Mechanisms that inhibit distal lung growth are poorly understood. Adrenomedullin (AM), a recently discovered potent vasodilator, promotes angiogenesis and has protective effects on the cardiovascular and respiratory system. Its role in the developing lung is unknown. We hypothesized that AM promotes lung angiogenesis and alveolar development. Accordingly, we report that lung mRNA expression of AM increases during normal alveolar development. In vivo, intranasal administration of the AM antagonist AM22-52 decreases lung capillary density (12.4±1.5 vs 18±1.5 in controls, p<0.05) and impairs alveolar development (mean linear intercept, MLI 52.3±1.5 vs 43.8±1.8, p<0.05 and septal counts 62.0±2.7 vs 90.4±3.5, p<0.05) in neonatal rats resulting in larger and fewer alveoli, reminiscent of BPD. This was associated with decreased lung eNOS and VEGF-A mRNA expression. In experimental oxygen-induced BPD, a model of arrested lung vascular and alveolar growth, AM attenuates arrested lung angiogenesis (vessel density 6.9±1.1 vs 16.2±1.3, p<0.05) and alveolar development (MLI 51.9±3.2 vs 44.4±0.7, septal counts 47.6±3.4 vs 67.7±4.0, p<0.05), an effect in part mediated by inhibition of apoptosis. AM also prevents pulmonary hypertension in this model, as assessed by decreased right ventricular hypertrophy and pulmonary artery medial wall thickness. Our findings suggest a role for AM during normal alveolar development. AM may have therapeutic potential in diseases associated with alveolar injury.