NALOXONE DISINHIBITS MAGNOCELLULAR RESPONSES TO OSMOTIC AND VOLEMIC STIMULI IN CHRONICALLY HYPOOSMOLAR RATS

Normonatremic and chronically hyponatremic rats were pretreated with n aloxone (5 mg/kg) or isotonic (150 mM) NaCl, then were given i.v. inje ctions of 2 M NaCl (2 ml) or were hemorrhaged (20 ml/kg). Baseline and post-stimulus blood samples were withdrawn through indwelling jugular venous catheters. Baseline levels of plasma vasopressin (AVP) and oxy tocin (OT) were similar in both normonatremic and hyponatremic rats an d did not change after naloxone pretreatment. Increases in plasma AVP and OT levels in response to both hypertonic saline and hemorrhage wer e markedly blunted in the hyponatremic rats compared to the normonatre mic rats. Naloxone pretreatment caused augmented AVP and OT secretion in response to hypertonic saline stimulation and hemorrhage in both th e normonatremic and hyponatremic rats; the magnitude of the naloxone a ugmentations in the hyponatremic rats were sufficient to normalize the OT response to hypertonic saline and both the OT and AVP responses to hemorrhage. Our results therefore suggest that endogenous opioids are likely involved in the inhibition of stimulus-induced AVP and OT rele ase that accompanies chronic hypoosmolality.