Hypoxia during pregnancy induces several responses at cardiovascular, endocrine and neurologic levels, which may derive in acute and chronic diseases. This is relevant in human populations exposed to high altitude, in either chronic continuous (permanent inhabitants) or intermittent fashion (high altitude workers and tourists). Further, it is estimated that 3% of the lowlands pregnancies suffer some degree of intrauterine hypoxia. Considering both populations, about 4-5 million babies/year are born from a hypoxic pregnancy in the world. Chronic intrauterine hypoxia during pregnancy induces oxidative stress, which in turn may promote cellular responses and epigenetic modifications resulting in severe impairment in growth and development. Sadly, this condition is accompanied with intrauterine growth restriction and increased fetal and neonatal morbi-mortality. Further, developmental hypoxia may program systems dysfunction later in postnatal life, ending in structural and functional alterations with augmented risk on neurological, metabolic and cardiovascular failures. The mechanisms involve determining the immediate, short and long-lasting effects are still unclear, but the lack of oxygen and increased oxidative stress are apparently triggering most of the responses. For several years, the study of the responses to hypoxic insults and pharmacological targets has been the motivation of our group. This talk will describe some of the mechanisms underlying the cardiovascular responses to hypoxia in the perinatal period and potential therapeutic approaches to diminish these effects. In the current worldwide scenario, where births and life expectancy are increasing, the Developmental Origins of Health and Disease (DOHaD) mechanisms demands urgently new treatments to deal with intrauterine hypoxia.