Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Control of aldosterone responsiveness in terminal renal failure. Plasma aldosterone concentration in 30 hemodialysis patients correlated closely with renin concentration, renin activity or renin and potassium concentrations combined (r is greater than or equal to 0.62; P is less than 0.01), and increased consistently in response to upright posture or corticotropin administration. Aldosterone response to hemodialysis was variable. Significant correlations (r is greater than or equal to 0.65; P is less than 0.01) were demonstrated between postural plasma aldosterone and renin responses, between aldosterone responses to corticotropin and basal plasma aldosterone or renin and potassium values, between hemodialysis-induced changes in plasma aldosterone and those in potassium or renin; but not between various indexes of heparin treatment and aldosterone activity. Bilateral nephrectomy reduced basal plasma renin and aldosterone concentrations and aldosterone responsiveness in five preoperatively normoreninemic or hyperreninemic patients, but not in a hyporeninemic patient. These results demonstrate the complementary roles of circulating renin and potassium in the control of aldosterone release under basal and stimulatory conditions in patients with terminal renal failure. Administration of heparin in dosages used during long-term hemodialysis does not appear to significantly interfere with aldosterone control.
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PMID:Control of aldosterone responsiveness in terminal renal failure. 16 31

The pathophysiologic effects of cocaine on neuronal, pulmonary, and cardiovascular tissue are related to the drug's interaction with select catecholamine and neuroendocrine systems. Cocaine has been shown to alter circulating levels of the neurotransmitters, dopamine, norepinephrine, epinephrine, as well as the hypothalamic-pituitary-adrenal axis hormones corticotropin-releasing factor (CRF), adrenocorticotropic hormone (ACTH), and cortisol. Furthermore, brain and lung tissue have been identified as primary sites of cocaine sequestration and metabolism. This paper reviews evidence suggesting that steroid-potentiated actions of catecholamines on vascular tissues contributes to the etiology of cocaine-related medical complications, including ischemic stroke, coronary ischemia, and ischemia-based renal failure.
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PMID:Brain, lung, and cardiovascular interactions with cocaine and cocaine-induced catecholamine effects. 133 74

Two dogs with idiopathic chylothorax and 2 dogs with experimentally induced (ie, ligation of the cranial vena cava) chylothorax were treated by intermittent thoracic drainage. Of these 4 dogs, 3 that did not have evidence of renal failure had normal or near-normal serum sodium and potassium concentrations before thoracic drainage began, and all 3 developed repeatedly marked hyponatremia and hyperkalemia during thoracic drainage. Another dog became weak and depressed, ostensibly because of hyperkalemia. Serum sodium and potassium concentrations in 1 dog with spontaneous chylothorax returned to normal after chylothorax resolved and thoracic drainage was stopped. The other 3 dogs died or were euthanatized, and the effect of stopping thoracic drainage could not be evaluated. In 3 dogs in which it was measured, normal-to-high plasma cortisol concentration was observed before and after adrenocorticotropin administration, and 2 dogs also had hyperaldosteronemia. Hyponatremia was hypothesized to be caused by sodium loss via thoracic drainage whereas hyperkalemia may have been multifactorial in origin, but probably was attributable, at least, in part to decreased renal potassium clearance.
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PMID:Hyponatremia and hyperkalemia associated with idiopathic or experimentally induced chylothorax in four dogs. 191 42

Plasma concentrations of glucose, insulin, and beta-endorphin/beta-lipotropin were measured in male Sprague-Dawley rats with experimental renal failure after intravenous glucose challenge in the presence and absence of opioid blockade with intravenously administered naloxone. The results were compared with those obtained in sham-operated normal control and pair-fed groups of animals. Baseline glucose concentrations were similar in the three groups of animals. Plasma baseline insulin concentrations were significantly lower in the rats with renal failure and the pair-fed animals compared with the normal controls. After glucose challenge the renal failure group demonstrated glucose intolerance, which was not improved after naloxone treatment given 15 minutes before glucose challenge. Peak insulin levels after glucose challenge in the renal failure and pair-fed groups increased significantly after naloxone administration. Interestingly, circulating concentrations of plasma beta-endorphin/beta-lipotropin were not significantly different in the three groups of animals when measured either in the baseline state or after glucose challenge. The data indicate that the carbohydrate intolerance in experimental renal failure may be partly due to an increase in pancreatic islet opioidergic tone, because an improvement in insulin secretion was demonstrated in the absence of any change in circulating beta-endorphin/beta-lipotropin concentrations after naloxone. The failure to demonstrate any improvement in glucose disposal after naloxone, despite the augmented secretion of insulin after naloxone in the animals with renal failure, points to peripheral resistance to the effects of insulin that is not influenced by opioid blockade.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glucose intolerance in renal failure: role of endogenous opioids. 214 12

Based on the analysis of a RX-ray study and a selective blood test for the activity of the plasma renin, aldesterone, hydrocortisone and adrenocorticotropic hormone (ACTH) in 57 patients with arterial hypertension--14 persons without renal failure, 14 ones regularly treated by hemodialysis, 29 patients with left orthostatic varicocele--the authors demonstrated the impact of the renal arterio- and phlebography on the hormone levels studied. Arteriography resulted in an increase in the absolute value of the renal vein renin mean 2.1-fold, aldosterone, 3.3-fold and hydrocortisone, 1.7-fold. A 2.2-fold increase in the renin activity and a 2.6-fold increase in the levels of aldosterone and hydrocortisone noted in all the patients were the result of retrograde renal phlebography. No correlations were established between the changes in hormone levels and the central mechanism of the secretion regulation (ACTH). Radiopaque investigations of the patients with arterial hypertension gave 22 per cent of false positive results with regard to the site of renin secretion and 18 per cent of those with regard to the participation of the studied kidney in renin secretion. The authors supposed a possible regulation of adrenal mineralocorticoid performance by a retrograde blood flow appeared through the adrenal central veins that was induced by phlebography--related elevation of blood pressure in the renal vein.
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PMID:[The effect of renal arterio- and phlebography on the function of the renin-angiotensin and hypophyseal-adrenal systems]. 218 46

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.
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PMID:Effects of naloxone administration on endocrine abnormalities in chronic renal failure. 303 7

Several alterations are present in the hypothalamic hypophyseal regulation of many hormones in patients with chronic renal failure. Evaluation of the hypothalamic hypophyseal adrenal axis in these groups of patients demonstrated normal levels of plasma cortisol. Dexamethasone suppression is abnormal after administration of 1 mg of oral dexamethasone, but normal after 3 mg. Dexamethasone blood levels were lower than the control after administration of 1 mg of oral dexamethasone. A dexamethasone metabolic clearance showed a similar half-life between the patients and controls. Oral absorption study showed poor absorption of the drug. Therefore, there is a problem of gastrointestinal absorption producing the abnormal dexamethasone suppression test in patients with renal failure. Results of metyrapone tests were normal. Corticotropin stimulation tests elicited a normal response. Insulin-induced hypoglycemia does not produce an increment in plasma cortisol or adrenocorticotropic hormone levels.
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PMID:Evaluation of the hypothalamic hypophyseal adrenal axis in patients receiving long-term hemodialysis. 628 45

In order to know the prevalence rate of adrenal insufficiency among patients with renal failure due to amyloidosis; we have performed a stimulation test with synthetic corticotropin hormone (Nuvacthen test) in nine patients diagnosed of renal amyloidosis and in five controls. We also measured ACTH and plasma cortisol levels. In two out of nine patients (22%) a low ACTH, low plasmatic cortisol and an abnormal response to Nuvacthen test were detected being diagnosed of primary adrenal insufficiency. We conclude that adrenal insufficiency is not an infrequent finding in systemic amyloidosis and may be due to secondary amyloidotic infiltration of adrenal or pituitary glands. Though Nuvacthen test is a useful test to diagnose subclinical adrenal insufficiency, in our series patients with an abnormal response also had low levels of basal cortisol and ACTH and no one patient with normal basal levels had an abnormal response to the stimulation test.
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PMID:[Adrenal insufficiency in patients with kidney failure secondary to amyloidosis. Its detection by a stimulation test]. 773 87

Microencapsulated genetically engineered cells have the potential to treat a wide range of diseases. For example, in experimental animals, implanted microencapsulated cells have been used to secrete growth hormone to treat dwarfism, neurotrophic factors for amyotrophic lateral sclerosis, beta-endorphin to decrease pain, factor XI for hemophilia B, and nerve growth factors to protect axotomized neurons. For some applications, microencapsulated cells can even be given orally. They can be engineered to remove unwanted molecules from the body as they travel through the intestine, and are finally excreted in the stool without being retained in the body. This application has enormous potential for the removal of urea in kidney failure, ammonia in liver failure and amino acids such as phenylalanine in phenylketonuria and other inborn errors of metabolism.
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PMID:Therapeutic uses of microencapsulated genetically engineered cells. 961 2

Lipoprotein(a) [Lp(a)], a strong independent cardiovascular risk factor, consists of the unique apolipoprotein(a) [apo(a)] covalently linked to a low-density lipoprotein particle. Apo(a) contains a widely differing number of the plasminogen-like kringle IV, a size polymorphism that is codominantly inherited. In addition to powerful genetic control, renal failure is known to influence the plasma Lp(a) concentration. There is still a lot to be learned about the mode and site of catabolism of Lp(a), and there is no readily applicable Lp(a)-lowering treatment available. Therefore, it was of interest to study further the Lp(a)-lowering effect of corticotropin (ACTH) that has been demonstrated in small studies. The main purpose of the present study was to investigate the influence of ACTH on different apo(a) isoforms. Short-term treatment with ACTH decreased the plasma Lp(a) concentration in all 26 study participants. The two study groups (12 healthy individuals and 14 hemodialysis patients) responded similarly, with a median decrease in plasma Lp(a) of 39% and 49%, respectively. In subjects with two clearly separable apo(a) bands, apo(a) phenotyping and densitometric scanning of the bands before and after treatment with ACTH revealed a change in the proportion of apo(a) isoforms, ie, a shift toward the isoform with lower molecular weight. This was observed in seven of nine investigated subjects (four of five healthy individuals and three of four hemodialysis patients).
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PMID:Corticotropin-induced reduction of plasma lipoprotein(a) concentrations in healthy individuals and hemodialysis patients: relation to apolipoprotein(a) size polymorphism. 1009 11


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