naloxone has been researched along with Endocrine-System-Diseases* in 5 studies
5 other study(ies) available for naloxone and Endocrine-System-Diseases
Article | Year |
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Serotonin 2A receptors modulate tail-skin temperature in two rodent models of estrogen deficiency-related thermoregulatory dysfunction.
Menopause-associated thermoregulatory dysfunction, including hot flushes and night sweats, is effectively treated by hormonal therapies that include estrogens. Evidence suggests that estrogen regulates serotonin 2A (5-HT(2A)) receptor expression and that 5-HT(2A) receptors are involved in thermoregulation. Therefore, the role of 5-HT(2A) receptors in thermoregulation was assessed in two rat models of ovariectomy-induced thermoregulatory dysfunction. The first model is based on measurement of the tail-skin temperature (TST) increase following naloxone-induced withdrawal in morphine-dependent ovariectomized (OVX) rats (MD model), while the second model relies on telemetric assessment of diurnal TST changes in ovariectomized rats (telemetry model). Treatment with a 5-HT(2A/2C) receptor agonist, (-)-2,5-dimethoxy-4-iodoamphetamine hydrochloride (DOI), prevented the naloxone-induced TST increase in the MD model and restored normal active-phase TST in the telemetry model. The selective 5-HT(2A) receptor antagonist, MDL-100907, had no effect on the naloxone-induced flush when administered alone in the MD model, but it decreased DOI's ability to abate the flush. In the telemetry model, MDL-100907 attenuated the DOI-induced decrease in active-phase TST. Interestingly, MDL-100907 increased TST in both models when given alone, with the TST increase occurring prior to the naloxone-induced flush in the MD model. To evaluate the role of central nervous system (CNS) 5-HT(2A) receptors in TST regulation, DOI was administered in combination with a known peripheral 5-HT(2A/2C) receptor antagonist, xylamidine, in the MD model. Xylamidine had no effect on DOI's ability to abate the naloxone-induced flush. These results indicate that activation of central 5-HT(2A) receptors restores temperature regulation in two rodent models of ovariectomy-induced thermoregulatory dysfunction. Topics: Amidines; Amphetamines; Animals; Disease Models, Animal; Dose-Response Relationship, Drug; Drug Interactions; Endocrine System Diseases; Estradiol; Estrogens; Female; Fluorobenzenes; Naloxone; Ovariectomy; Piperidines; Rats; Reaction Time; Receptor, Serotonin, 5-HT2A; Serotonin Antagonists; Serotonin Receptor Agonists; Skin Temperature; Substance Withdrawal Syndrome; Telemetry; Time Factors | 2004 |
Effect of naloxone on endocrine abnormalities in acute renal failure.
Topics: Acute Kidney Injury; Adrenocorticotropic Hormone; Adult; Calcitonin; Endocrine System Diseases; Female; Follicle Stimulating Hormone; Gonadotropin-Releasing Hormone; Growth Hormone; Humans; Insulin; Insulin Secretion; Luteinizing Hormone; Male; Naloxone; Parathyroid Hormone; Prolactin; Receptors, Opioid | 1988 |
Effects of naloxone administration on endocrine abnormalities in chronic renal failure.
In 72 patients with end-stage renal failure and 70 healthy subjects, the influence of blockade of opioid receptors by naloxone on secretion of prolactin, lutropin (LH), follitropin (FSH), adrenocorticotropin (ACTH), somatotropin (HGH), insulin (IRI), glucagon (IR-G), parathyroid hormone (PTH) and calcitonin (CT) was studied. Administration of naloxone stimulated luliberin-induced LH and FSH secretion quantitatively equally in patients and controls. Blockade of opioid receptors was followed by a less marked suppression of chlorpromazine-induced prolactin secretion but by a higher response of hypoglycemia-induced ACTH secretion in uremic patients than in controls. In addition, a less marked suppressive effect of naloxone was noted on hypoglycemia-induced HGH secretion in chronic renal failure as compared with controls. Blockade of opioid receptors improved significantly glucose tolerance and glucose-induced insulin secretion in uremic patients and suppressed nearly completely glucagon secretion response during the second phase of a glucose tolerance test. Finally, administration of naloxone was followed by a blunted response of Ca-induced CT secretion and suppression of PTH. Data presented in this paper suggest the existence of hyperendorphinism in end-stage renal failure. Topics: Calcitonin; Endocrine System Diseases; Glucagon; Humans; Insulin; Insulin Secretion; Kidney Failure, Chronic; Male; Naloxone; Parathyroid Hormone; Pituitary Hormones, Anterior; Receptors, Opioid | 1987 |
[The endocrine system and shock].
Topics: Diabetes Complications; Diabetic Coma; Drug Combinations; Endocrine System Diseases; Glucose; Humans; Hyperthyroidism; Insulin; Male; Middle Aged; Naloxone; Potassium; Shock; Somatostatin; Thyroid Hormones | 1982 |
Hypothalamic amenorrhea in runners of normal body composition.
Three amenorrheic runners of normal body weight, in whom organic disease had been excluded, were found to exhibit: (1) normal body composition, (2) low baseline concentrations of serum LH and normal concentrations of FSH, (3) normal to hyper-responsiveness of LH and FSH to GnRH testing, and (4) normal and possibly increased frequency of LH pulsations. In one of the 3 runners, the administration of naloxone was followed by a pronounced increase in the amplitude of the LH pulsations. Topics: Adolescent; Adult; Amenorrhea; Body Composition; Endocrine System Diseases; Estradiol; Female; Follicle Stimulating Hormone; Humans; Hypothalamus; Luteinizing Hormone; Naloxone; Pituitary Hormone-Releasing Hormones; Running; Sports Medicine | 1980 |