Naloxone disinhibits magnocellular responses to osmotic and volemic stimuli in chronically hypoosmolar rats.
Normonatremic and chronically hyponatremic rats were pretreated with naloxone (5 mg/kg) or isotonic (150 mM) NaCl, then were given i.v. injections 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 Baseline and post-stimulus blood samples were withdrawn through indwelling jugular venous catheters.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 oxytocin (OT) were similar in both normonatremic and hyponatremic rats and did not change after naloxone pretreatment. Increases in plasma AVP and OT levels in response to both hypertonic saline and hemorrhage were markedly blunted in the hyponatremic rats compared to the normonatremic rats. Naloxone pretreatment caused augmented AVP and OT secretion in response to hypertonic saline stimulation and hemorrhage in both the normonatremic and hyponatremic rats; the magnitude of the naloxone augmentations 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 release that accompanies chronic hypoosmolality.
Dohanics
J
J
Department of Medicine, University of Pittsburgh, PA 15261, USA.
Verbalis
J G
JG
D000818:Animals; D001127:Arginine Vasopressin / Q000378:metabolism; D002543:Cerebral Hemorrhage / Q000378:metabolism*; D007031:Hypothalamus / Q000187:drug effects / Q000378:metabolism*; D007552:Isotonic Solutions / Q000494:pharmacology; D008297:Male; D009270:Naloxone / Q000494:pharmacology*; D009994:Osmolar Concentration; D010121:Oxytocin / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000097:blood; D012965:Sodium Chloride / Q000494:pharmacology; D014883:Water-Electrolyte Imbalance / Q000378:metabolism*
D007552:Isotonic Solutions; D001127:Arginine Vasopressin; D009270:Naloxone; D012965:Sodium Chloride; D010121:Oxytocin; D012964:Sodium