Abstract Inhibition of hypoxia signalling leads to respiratory distress syndrome (RDS) whilst administration of vascular endothelial growth factor (VEGF), the most widely characterised hypoxia responsive factor, protects from RDS. In the lung of the chronically hypoxemic placentally restricted (PR) fetus, there is altered regulation of hypoxia signalling. This leads to reduced surfactant maturation in late gestation and provides evidence for increased risk of RDS in growth restricted neonates at birth. We evaluated the effect of recombinant human VEGF administration to bypass endogenous regulation of hypoxia signalling in the lung of the normally grown and PR sheep fetus. There was no effect of VEGF administration on fetal blood pressure or fetal breathing movements. We examined the effect on expression of genes regulating VEGF signalling (FLK and KDR), angiogenesis (ANGTP1, AQP1, ADM), alveolarisation (MMP2, MMP9, TIMP1, COL1A1, ELN), proliferation (IGR1, IGF2, IGF1R, MKI67, PCNA), inflammation (CCL2, CCL4, IL1B, TNFA, TGFB1, IL10) and surfactant maturation (SFTP‐A, SFTP‐B, SFTP‐C, SFTP‐D, PCYT1A, LPCAT, LAMP3, ABCA3). Despite effects of PR on expression of genes regulating airway remodelling, inflammatory signalling and surfactant maturation, there were very few effects of VEGF administration on gene expression in the lung of both the normally grown and PR fetus. There were, however, positive effects of VEGF administration on the percent tissue, air space and numerical density of SFTP‐B positive alveolar epithelial cells in fetal lung tissue. These results provide evidence for stimulatory effects of VEGF administration on structural maturation in the lung of both the normally grown and PR fetus. This article is protected by copyright. All rights reserved