Abstract
Hypoxic-stress is a potent stimulator of in utero meconium passage in term human and rat fetuses. Together with known corticotrophin releasing factor (CRF) gastrointestinal (GI) stimulatory effects and elevated CRF levels in hypoxic rat fetuses, we propose that CRF is a key mediator of hypoxia-induced fetal meconium passage. As CRF action is mediated by binding to GI stimulatory R1 receptors, we sought to determine the presence of CRF-R1 in the GI tracts of term rat fetuses by anatomical and biochemical techniques.
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