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.
D002116:Calcitonin / Q000378:metabolism; D004700:Endocrine System Diseases / Q000503:physiopathology*; D005934:Glucagon / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D007676:Kidney Failure, Chronic / Q000150:complications*; D008297:Male; D009270:Naloxone; D010281:Parathyroid Hormone / Q000378:metabolism; D010908:Pituitary Hormones, Anterior / Q000378:metabolism; D011957:Receptors, Opioid / Q000503:physiopathology*
D007328:Insulin; D010281:Parathyroid Hormone; D010908:Pituitary Hormones, Anterior; D011957:Receptors, Opioid; D009270:Naloxone; D002116:Calcitonin; D005934:Glucagon