Naloxone decreases the inhibiting effect of ethanol on the release of arginine-vasopressin induced by cigarette smoking in man.
In order to establish whether ethanol exerts its inhibiting effect on the nicotine-induced release of arginine-vasopressin (AVP) by interacting with an opioid pathway, six normal volunteers were treated with naloxone (2 or 4 mg as IV bolus, plus 5 or 10 mg infused over 105 minutes) during (2 nonfilter) cigarette smoking and ethanol (50 mL to 110 mL of whiskey) drinking. In addition, control experiments with naloxone, ethanol, or cigarette smoking alone were performed. When given alone, naloxone and ethanol did not modify AVP secretion, whereas nicotine increased plasma AVP levels by about 2.5-fold. This effect was completely blocked by ethanol. In the presence of naloxone, AVP rose only by about 1.7-fold in response to nicotine. Since naloxone only partially reversed the inhibiting effects of ethanol, only a partial involvement of opioid peptides in ethanol action might be supposed. Alternatively, ethanol and naloxone-sensitive opioids might produce their inhibiting effects on AVP rise in response to nicotine through independent pathways.
D000328:Adult; D001127:Arginine Vasopressin / Q000378:metabolism*; D000431:Ethanol / Q000037:antagonists & inhibitors* / Q000494:pharmacology; D005260:Female; D006801:Humans; D008297:Male; D009270:Naloxone / Q000494:pharmacology*; D009538:Nicotine / Q000494:pharmacology; D012907:Smoking
D001127:Arginine Vasopressin; D009270:Naloxone; D000431:Ethanol; D009538:Nicotine