Abstract
In all vertebrates, hypoxia plays an important role in fetal development, driving vasculogenesis, angiogenesis, hematopoiesis, and chondrogenesis. Therefore, the ability to sense and respond to changes in the availability of oxygen (O(2)) is crucial for normal embryonic development as well as for developmental plasticity. Moderate levels of hypoxia trigger a regulated process which leads to adaptive responses. Regulation of angiogenesis by hypoxia is an important component of homeostatic control mechanisms that link the cardio-pulmonary-vascular O(2) supply to metabolic demands in local tissues. Hypoxia leads to the activation of genes that are important for cell and tissue adaptation to low O(2) conditions, such as hypoxia-inducible factor 1. Previous studies have shown a dose-response effect to hypoxia in chicken embryos, with lower and/or prolonged O(2) levels affecting multiple mechanisms and providing a spectrum of responses that facilitate the ability to maintain O(2) demand despite environmental hypoxia. In chicken embryos, mild to extreme hypoxia during embryogenesis improves chorioallantoic membrane and cardiovascular development, resulting in an increase in O(2) carrying capacity and leading to developmental plasticity that may affect post-hatch chick performance and improve adaptation to additional environmental stresses at suboptimal environmental conditions.