Effects of Naloxone Administration on Endocrine Abnormalities in Chronic Renal Failure

Abstract

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.

Influence of Type of Immunosuppressive Therapy on Secretion of Somatotropin and Function of the Pituitary-Adrenal and Pituitary-Gonadal Axis in Patients with a Kidney Transplant

“…Data shown in this paper suggest that the presence of a functioning kidney transplant does not normalize ele vated basal STH plasma levels which occur in chronic uremic patients [4,9], In addition a kind of immunosup pressive therapy exerts a significant influence on hypo glycemia-induced STH secretion. The response of STH secretion to hypoglycemia was significantly suppressed in patients of the azathioprine group as compared with normals and patients treated with ciclosporin.…”

“…All hormones were assessed by radioimmunoassay according to Grzeszczak et al [4] and Kokot and Stupnicki [11], and creatinine by the routine picric-acid method. …”

“…16]. Among them, abnormal secretion of somatotropin (STH) [4,9] and dysfunction of the pituitary-adrenal [3,4,17,18] and pituitary-gonadal axis [5,10,[12][13][14] are to be mentioned. After successful renal transplantation, most but not all of the above-mentioned endocrine abnormalities are absent or improved in patients receiving conventional immuno suppressive therapy [azathioprine + prednisone; 7, 8,13].…”

Elevated Plasma Levels of Opioid Peptides and Delta Sleep-Inducing Peptide but Not of Corticotropin-Releasing Hormone in Patients Receiving Chronic Hemodialysis

“…The responses to stimulation and suppres sion tests in various endocrine systems are markedly affected in uremic patients by a blockade of opioid receptors with naloxone [33] . Furthermore, a decrease in the plasma levels of p-END together with a decrease in the plasma levels of growth hormone and parathyroid hormone have been described in patients on a low-protein diet [27].…”

Effects of a Low-Phosphorus, Low-Nitrogen Diet Supplemented with Essential Amino Acids and Ketoanalogues on Serum Beta-Endorphin in Chronic Renal Failure

“…High levels of these polypeptides are indeed known to stimulate the secretion of parathyroid hormone (PTH) [I],growth horm one(G H ) [2.3], pituitary thyroid-stimulating hormone (TSH) [2], gonadotropins (LH. FSH) [4,5], prolactin (PRL) [2] and to cause glucose intolerance [6]. Circulating P-endorphin ((3-EP) is high in CRF and this is the most active of these compounds [7], Some years ago a very low-protein diet supplemented with essential amino acids and ketoanalogues (supple mented diet, SD) was introduced in the treatment of severe C R F [8) and it was found that it can slow down the rate of decline of the residual renal function [8,9], reverse secondary hyperparathyroidism [10,II], improve TSH and Tj levels [12], and restore gonadal testosterone (T) secretion in males [13].…”