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Neutrophil function and opioid receptor expression on leucocytes during chronic naltrexone treatment in humans.
- Source :
-
Pharmacological research [Pharmacol Res] 1999 Aug; Vol. 40 (2), pp. 153-8. - Publication Year :
- 1999
-
Abstract
- We report that neutrophil function was impaired in former heroin addicts on chronic naltrexone maintenance. Of the subjects, 62.5% had elevated plasma ACTH, 25% had elevated plasma cortisol and one subject had increased urinary cortisol. All subjects showed enhanced expression of opioid receptors on monocytes, neutrophils and lymphocytes. In vitro, incubation with therapeutically relevant concentrations of naltrexone induced a slow increase of neutrophil cytoplasmatic free Ca(2+)concentrations ([Ca(2+)]()E2>i) and slowed down the [Ca(2+)]()E2>i rise induced by N-formyl-methionyl-leucyl-phenylalanine. Neither naltrexone nor its metabolite beta-naltrexol affected human neutrophil function in vitro. We conclude that impairment of neutrophil function during chronic naltrexone may be related to opioid receptor overexpression. With this regard, the possible role of naltrexone-induced [Ca(2+)]()E2>i changes deserves further investigation. 1999 Academic Press.<br /> (Copyright 1999 Academic Press.)
- Subjects :
- Adolescent
Adrenocorticotropic Hormone blood
Adrenocorticotropic Hormone drug effects
Adult
Calcium metabolism
Female
Heroin Dependence drug therapy
Humans
Hydrocortisone blood
Hydrocortisone urine
Leukocytes cytology
Leukocytes metabolism
Male
Naltrexone analogs & derivatives
Naltrexone pharmacology
Neutrophils metabolism
Neutrophils physiology
Receptors, Opioid biosynthesis
Leukocytes drug effects
Naltrexone therapeutic use
Narcotic Antagonists therapeutic use
Neutrophils drug effects
Receptors, Opioid drug effects
Subjects
Details
- Language :
- English
- ISSN :
- 1043-6618
- Volume :
- 40
- Issue :
- 2
- Database :
- MEDLINE
- Journal :
- Pharmacological research
- Publication Type :
- Academic Journal
- Accession number :
- 10433874
- Full Text :
- https://doi.org/10.1006/phrs.1999.0488