naloxone and Thymoma

naloxone has been researched along with Thymoma* in 2 studies

Other Studies

2 other study(ies) available for naloxone and Thymoma

ArticleYear
The kappa opioid receptor expressed on the mouse R1.1 thymoma cell line down-regulates without desensitizing during chronic opioid exposure.
    The Journal of pharmacology and experimental therapeutics, 1995, Volume: 272, Issue:3

    The R1.1 mouse thymoma cell line expresses a single class of kappa opioid receptors that is negatively coupled to adenylyl cyclase through a Bordetella pertussis toxin-sensitive inhibitory guanine nucleotide-binding protein. The aim of the present study was to determine whether chronic opioid treatment of R1.1 cells altered either the binding properties or the functional response associated with the kappa opioid receptor. Culturing of R1.1 cells with the kappa-selective agonist (trans)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl] benzeneacetamide methane-sulfonate hydrate (U50,488) for 3 hr and longer, followed by extensive washing of R1.1 cell membranes, produced a concentration- and time-dependent reduction in the binding of the kappa-selective ligand (5 alpha,7 alpha,8 beta)-(-)-N-methyl-N-(7-(1-pyrrolidinyl)-1- oxaspiro(4,5)dec-8-yl) benzeneacetamide ([3H]U69,593). Culturing of R1.1 cells with 100 nM U50,488 for 24 hr produced approximately a 50% reduction in the Bmax value for [3H]U69,593 and [3H]naloxone binding. In contrast to the reduction in binding, there was no change in the inhibition of adenylyl cyclase activity by (-)-U50,488. To determine whether kappa opioid receptor function was maintained by spare receptors after agonist-induced down-regulation, membranes from untreated R1.1 cells were incubated with 400 nM of the irreversible opioid antagonist beta-chlornaltrexamine (beta-CNA) followed by extensive washing. beta-CNA produced a 50% reduction in the [3H]U69,593 binding and a 6-fold increase in the IC50 value for (-)-U50,488 inhibition of adenylyl cyclase activity, with no change in the maximal inhibition of cyclic AMP levels.(ABSTRACT TRUNCATED AT 250 WORDS)

    Topics: 3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer; Adenylate Cyclase Toxin; Adenylyl Cyclases; Animals; Benzeneacetamides; Cell Membrane; Down-Regulation; In Vitro Techniques; Mice; Naloxone; Naltrexone; Pertussis Toxin; Pyrrolidines; Receptors, Opioid, kappa; Thymoma; Tumor Cells, Cultured; Virulence Factors, Bordetella

1995
Concomitant suppression of plasma ACTH- and beta-endorphin-like immunoreactivity by cyproheptadine, naloxone, and somatostatin in the ectopic ACTH syndrome.
    Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme, 1985, Volume: 17, Issue:4

    Release of plasma ACTH- and beta-endorphin (beta-EP)-like immunoreactivity (LI) was studied in vivo in a patient with an ectopic ACTH-producing malignant thymoma. Administration of lysin vasopressin stimulated concomitant release of plasma ACTH- and beta-EP-LI. Administration of cyproheptadine, naloxone, and somatostatin significantly suppressed plasma levels of ACTH- and beta-EP-LI, while saline infusion did not. Gel exclusion chromatography of the plasma extracts revealed that ACTH-LI consisted of two components, large and small molecular weight form, while beta-EP-LI consisted of three components, large molecular weight, beta-lipotropin-, and beta-EP-sized form; each of these components was incompletely suppressed by somatostatin infusion. It is suggested that certain tumors may have acquired aberrant multiple receptors during malignant transformation which may lead to the paradoxical hormone response as demonstrated in this case.

    Topics: ACTH Syndrome, Ectopic; Adrenocorticotropic Hormone; Adult; beta-Endorphin; Cyproheptadine; Endorphins; Humans; Lypressin; Male; Naloxone; Paraneoplastic Endocrine Syndromes; Somatostatin; Thymoma; Thymus Neoplasms

1985