Histaminergic H1 and H2 receptors do not mediate cortisol release in response to naloxone in normal men.
In order to evaluate the role of histamine as a possible mediator of the ACTH-cortisol response to naloxone, a specific opioid receptor antagonist, 12 normal men were treated with naloxone before and after the administration of dexchlorpheniramine and cimetidine, respectively H1 and H2 histamine receptor antagonists. Cortisol levels in the plasma were measured before and after drug injections. Naloxone significantly stimulated the secretion of cortisol in all subjects; the administration of dexclorpheniramine or cimetidine failed to modify this response. These data confirm the stimulatory effect of naloxone on cortisol secretion, but do not support the hypothesis that a histaminergic pathway mediates this response.
D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D002744:Chlorpheniramine / Q000494:pharmacology; D002927:Cimetidine / Q000494:pharmacology; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism*; D008297:Male; D009270:Naloxone / Q000494:pharmacology*; D011968:Receptors, Histamine / Q000502:physiology*; D011969:Receptors, Histamine H1 / Q000502:physiology*; D011970:Receptors, Histamine H2 / Q000502:physiology*; D013997:Time Factors
D011968:Receptors, Histamine; D011969:Receptors, Histamine H1; D011970:Receptors, Histamine H2; D009270:Naloxone; C018904:dexchlorpheniramine; D002744:Chlorpheniramine; D002927:Cimetidine; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone