Endogenous opioid peptides inhibit oxytocin release in the lactating rat after dehydration and urethane.

Abstract

One physiological role for endogenous opioid peptides is to attenuate the release of oxytocin (OT) from the hypothalamo-neurohypophysial system during dehydration and hemorrhage when vasopressin maintains fluid balance and blood pressure. During lactation, OT, which stimulates milk ejection, is released without vasopressin. The influence of endogenous opioid peptides on OT release during suckling has been studied primarily in animals anesthetized with urethane. In addition to anesthesia, urethane dehydrates the animal by elevating plasma osmolality and reducing cardiovascular volume. Thus, we examined in lactating rats the response of the magnocellular neuroendocrine system to dehydration and the role of endogenous opioid peptides in regulating OT release during suckling under conditions of altered fluid balance in conscious and urethane-anesthetized rats. Release of OT in response to an increase in plasma osmolality or a decrease in blood volume was attenuated during lactation in both conscious and anesthetized rats. Blockade of opiate receptors with naloxone (5 mg/kg) did not alter suckling-induced release of immunoreactive OT in conscious, normally hydrated rats, but did augment hormone release after urethane (1.1 g/kg, ip) or after osmotic stimulation with hypertonic sodium chloride (2.5%; 20 ml/kg, ip). During dehydration, the combination of decreased responsiveness of oxytocinergic neurons to osmotic stimulation and inhibition of OT release by opioid peptides may be important in the lactating rat for conserving pituitary stores of OT needed for milk ejection.