During the growth and developmental period, a developing embryo is sensitive to alterations and perturbation in the environment, such as nutritional insufficiencies and environmental inadequacies, that could potentially cause significant ramifications in the future growth and survivability of the organism as an adult. Prenatal stress is an important etiological factor in the onset of adult hypertension but the mechanisms responsible for this, and other related pathologies that may arise from the influence of environmental stress on an embryo, are poorly understood.

β adrenergic receptors (βAR) modulate the inotropic and chronotropic activity of the heart. Catecholamines mediate the regulation of cardiac performance through the positive stimulation of these receptors. Under periods of stress, such as exposure to hypoxic conditions during embryonic growth, chronic elevated levels of circulating plasma catecholamines hyperstimulate the βARs, triggering physiological changes in the heart. Mammalian and avian studies demonstrate that chronic prenatal hypoxia sensitizes βARs in the embryonic heart but causes postnatal desensitization.

A potential explanation for these differences in sensitivity is a shift in the relative expression of β₁AR and β₂ARs, measured with respect to the relative gene expression of these receptors in the cardiomyocytes of the developing embryos at different developmental ages. The purpose of this study is to investigate whether low fetal oxygen conditions have a programming affect on βAR signaling, by studying the changes in mRNA expression at different stages of development relative to embryos incubated under ambient oxygen level conditions. We postulate that the restriction of oxygen during embryonic development may cause an altered βAR subtype ratio in the heart, which in turn could potentially result in an altered contractile response.