Abstract
During fetal life, pituitary-adrenal function is regulated by a number of factors, including corticotropin-releasing factor, arginine vasopressin and opioid peptides. Using the fetal sheep as an animal model, we have found that morphine (2.5 and 5.0 mg/h) causes a significant increase in fetal plasma cortisol levels. Recent studies on the multiple subtypes of opioid receptors suggest that μ, δ, and κ receptors exert vastly different actions on many physiological systems. In this study, we compared the effects of μ- and δ-selective agonists as well as dynorphin-A(1–13) on fetal plasma cortisol levels. When administered to the fetal lateral ventricle, DAMGO (μ-selective) caused a significant increase in fetal plasma cortisol levels, while DPDPE and deltorphin (δ-selective) had no effect. Peripheral and central administration of dynorphin also caused an increase in fetal plasma cortisol which was not reversed by naloxone. These results suggest that opioid-induced increase in fetal plasma cortisol is mediated by μ receptors, most likely at the hypothalamic or pituitary level.
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