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)

An analysis of the factors that influence the increase in plasma immunoreactive beta-melanocyte-stimulating hormone (beta-MSH) concentration in chronic renal failure showed that: (a) the increase correlated with the increase in serum creatinine concentrations; (b) beta-MSH was not cleared from the plasma by haemodialysis; (c) beta-MSH concentrations increased with length of time on dialysis and increased further after bilateral nephrectomy but there was no further increase with time; (d) beta-MSH levels decreased to normal after renal transplantation; and (e) beta-MSH was excreted in urine only when plasma levels rose to well above those of chronic renal failure (in Nelson's syndrome). These findings suggest that the kidney regulated plasma beta-MSH by a non-excretory mechanism and is the major site of beta-MSH metabolism.
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PMID:Role of the kidney in regulating plasma immunoreactive beta-melanocyte-stimulating hormone. 76 7

beta-endorphin (BE) and other opioid peptides participate significantly in the development of the uremic syndrome. In patients with chronic renal failure (CRF) an elevated serum BE level and lack of a twenty-four-hour BE-secretory pattern were found. In 14 patients with CRF on conservative treatment with serum creatinine above 500 mumol/l and in 14 healthy subjects serum BE was evaluated after intravenous insulin injection. An adequate hypoglycemia was obtained in every subject. Basel serum BE concentration was significantly higher in patients with CRF than in healthy subjects and correlation positively with creatinine. After 60 min. from insulin injection in both groups the peak BE level was observed here after 120 min. it returned to the initial values. The curve of BE concentration in patients with CRF ran significantly higher than in healthy subjects. A total secretory answer of the pituitary measured by the area over basel value of BE was similar in both groups. It seems that BE secretion by the corticotropic cells of the pituitary is unchanged in patients with CRF. Impaired BE elimination by the kidneys is probably responsible for hyper-beta-endorphin levels in those patients.
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PMID:[Levels of beta-endorphin in serum of patients with chronic renal failure on conservative treatment during insulin-induced hypoglycemia stimulation testing]. 130 70

Plasma corticotropin-releasing hormone immunoreactivity (CRH IR) rises with gestational age in women. In order to investigate the physiological changes of the hormone in pregnant women's urine, CRH IR was measured by radioimmunoassay in urine collected over a 24-hour period, a blood sample and a subsequent single collection of urine after the 24-hour collection (spot urine). Plasma CRH IR in pregnant subjects, 8682.8 +/- 2063.0 pg CRH IR/ml plasma (mean +/- SEM, n = 25), was significantly higher than that in the non-pregnant controls (7.2 +/- 1.6 pg/ml, n = 5; separate t = 4.21, p = 0.0003, d.f. = 24). Similarly, pregnant women had higher spot urine CRH IR - 54.6 +/- 15.5 pg/mumol creatinine (Cr) versus 5.0 +/- 0.5 pg/mumol Cr (separate t = 3.20, p = 0.0038, d.f. = 24.0) - and 24-hour urine CRH IR - 13.7 +/- 1.2 pg/mumol Cr compared with 7.7 +/- 0.8 pg/mumol Cr (separate t = 4.28, p = 0.003, d.f. = 24.4) than the non-pregnant cohort. The difference between urinary excretion of CRH IR as estimated by 24-hour urine (13.7 +/- 1.2 pg/mumol Cr) and spot urine (54.6 +/- 15.5 pg/mumol Cr) indicated that CRH IR in 24-hour urine may be degraded during storage. The weak associations between plasma and 24-hour urine CRH IR of pregnant women (correlation coefficient r = 0.34, p greater than 0.1), and total 24-hour urine and spot urine CRH IR (r = 0.25, p less than 0.1) further indicate CRH degradation. Plasma and spot urinary CRH IR, however, were strongly correlated (r = 0.80, p = 0.001). The total CRH IR excreted as estimated from the spot urine value (0.5 +/- 0.1 micrograms/day) compared with the total filtered load of CRH IR in the pregnant group (1306.9 +/- 324.6 micrograms/day) showed that 99.97% of the filtered CRH IR was reabsorbed or metabolized by the kidneys. Acidic gel chromatography of spot and 24-hour urine samples showed a CRH IR peak at CRH41 standard elution position (Kd = 0.5), indicating that the molecular form in urine is similar to the 41-residue standard. Pregnancy-induced hypertension correlated positively with plasma CRH IR (r = 0.62, p less than 0.001) and spot urine CRH IR (r = 0.46, p less than 0.01), and negatively with parity (r = -0.60, p less than 0.001). Plasma CRH IR and parity also negatively correlated (r = -0.41, p less than 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Urinary corticotropin-releasing hormone immunoreactivity is elevated during human pregnancy. 208 19

One hundred male patients who presented with acute gouty arthritis were alternately assigned to 2 treatment groups. Seventy-six patients completed the study protocol, in which each gout attack during a 1-year period was treated. For each gout episode, 36 patients received a single intramuscular injection of 40 IU of adrenocorticotropic hormone (ACTH), and 40 patients received oral indomethacin, 50 mg 4 times daily with meals, until the pain abated. The time interval until the pain was relieved, as well as any untoward effects, were recorded for each gout attack treated. Both groups were of similar age, and had similar values for intercritical serum uric acid, 24-hour urinary uric acid, and creatinine clearance (1 month after entry into the study). The mean interval (+/- SD) to relief of pain was significantly shorter for the ACTH group (3 +/- 1 hours) than for the indomethacin group (24 +/- 10 hours). No side effects were noted in the ACTH group. However, of the 40 patients receiving indomethacin, 22 had abdominal discomfort of dyspepsia, 15 had headaches, and 12 had difficulty with mentation. Single-dose parenteral ACTH appeared to be effective more rapidly and was associated with fewer side effects than oral indomethacin in the treatment of acute gout.
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PMID:Comparison of parenteral adrenocorticotropic hormone with oral indomethacin in the treatment of acute gout. 245 35

Urinary levels of immunoreactive (IR) human NH2-terminal (hNT) of pro-opiomelanocortin were measured in 43 patients with various cell types of lung cancer (19 squamous cells, 12 oat cells, 2 large cells, and 10 adenocarcinoma), 32 patients with benign lung disease, two patients after hypophysectomy, and in 23 healthy volunteers. Lung cancer patients were divided into two subgroups according to the stage of the disease: 22 patients had "limited", and 21 patients "extensive" disease. Urinary and plasma levels were measured in 9 patients with lung cancer before and after radio- and chemotherapy or surgery. Urine samples were dialyzed and IR hNT material was extracted by Sep Pak C-18 cartridges using a propanol-2/TFA solvent system. The plasma and urinary IR hNT levels of the normal controls were 124 +/- 25 pg/ml and 47.8 +/- 14.5 pg/mg creatinine, respectively. The plasma levels of IR hNT were elevated (greater than mean + 2SD) in 65% of our patients with histologically proven lung cancer (422 +/- 775, mean +/- SD, pg/ml). The highest incidence of an elevated plasma level of IR hNT was found in oat cell carcinoma (83%). Elevated plasma IR hNT occurred in 66% of the patients with benign pulmonary disease (246 +/- 141 pg/ml, N.S.). In cancer patients with "limited" disease we found levels of 226 +/- 143 pg/ml and in patients with "extensive" disease 627 +/- 1074 pg/ml (N.S.). The urinary IR hNT level in lung cancer patients was 186 +/- 337 pg/mg creatinine and 81% of our patients had elevated levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Urinary levels of immunoreactive NH2-terminal of pro-opiomelanocortin in patients with malignant pulmonary disease. 253 37

The objective of this study was to determine the effects of transient aortic valve occlusion (balloon valvuloplasty) on vasoactive hormones in patients with heart failure. Plasma atrial natriuretic peptide, vasopressin, aldosterone, adrenocorticotropic hormone (ACTH), and plasma renin activity were measured before, immediately after, and 30 minutes and 18 to 24 hours following balloon inflation in 18 patients. Mean right atrial and pulmonary wedge pressures were 6 and 18 mm Hg before inflations, respectively, and were unchanged after balloon inflations (5 and 13 mm Hg, respectively). Systemic systolic/diastolic pressures were 139 +/- 8/65 +/- 4 mm Hg before occlusion, decreased to 47 +/- 5/34 +/- 3 mm Hg during occlusion, and returned to baseline after occlusions. Baseline atrial natriuretic peptide levels were 267 +/- 43 pg/ml and increased to 513 +/- 71 pg/ml after balloon inflations. Vasopressin levels before occlusion were 9.1 +/- 2.2 pg/ml and increased to 21.4 +/- 4.8 pg/ml after balloon inflations. Plasma renin activity was 5.4 +/- 1.4 ng/ml/hr before inflations and was not significantly changed after balloon inflations. No clinically significant changes in plasma sodium, potassium, creatinine, and osmolality were observed after the procedure. Aldosterone increased from 23 +/- 4 to 40 +/- 7 ng/dl 10 minutes after the last inflation. Plasma ACTH measured in seven patients with increased aldosterone was 28 +/- 8 pg/ml before and increased to 295 +/- 157 pg/ml 10 minutes after balloon inflations. The increases in natriuretic peptide and vasopressin were likely due to elevated intracardiac and decreased arterial pressures, respectively; they persisted in spite of no clinically significant changes in filling pressures 12 to 24 hours after the procedure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Stimulation of atrial natriuretic peptide and vasopressin during percutaneous transluminal aortic valvuloplasty. 254 14

Dogs with spontaneous pituitary-dependent hyperadrenocorticism were divided into two groups, one with normal plasma concentrations of alpha-MSH (normal alpha-MSH dogs, n = 26) and the other with high plasma concentrations of alpha-MSH (high alpha-MSH dogs, n = 14), on the presumption that high alpha-MSH concentrations indicated a parent cell of pars intermedia origin. The urinary corticoid/creatinine ratios of the high alpha-MSH dogs were significantly higher than those of the normal alpha-MSH dogs. The percentage decrease of the corticoid/creatinine ratios following dexamethasone administration was significantly higher in the normal alpha-MSH dogs than in the high alpha-MSH dogs. Dexamethasone resistance occurred in both the normal alpha-MSH dogs (4 out of 26) and the high alpha-MSH dogs (7 out of 14), indicating a relative rather than an absolute difference. The short-term effect of orally administered bromocriptine, at a dose (10 micrograms/kg body weight) known to be effective in lowering prolactin concentrations in dogs, was investigated by measuring concentrations of cortisol, ACTH and alpha-MSH in plasma at 4, 6 and 8 h after administration. Significant decreases were observed for cortisol in both groups and for alpha-MSH only in the high alpha-MSH dogs. The effect of 5 days of bromocriptine administration (10 micrograms at 12-h intervals) was assessed by measurements of urinary corticoid/creatinine ratios. Considering both groups as a whole, only the corticoid/creatinine ratios of the high alpha-MSH dogs decreased significantly on the first day of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of bromocriptine on corticotrophin, melanotrophin and corticosteroid secretion in dogs with pituitary-dependent hyperadrenocorticism. 284 49

Plasma met-enkephalin and leu-enkephalin has been measured in a group of 28 patients with chronic renal failure, to discover whether these opioids are affected by standard haemodialysis and haemofiltration. Met-enkephalin was markedly higher (P less than 0.001) in uraemic patients than in a group of 13 normal subjects, and was directly related to plasma creatinine (r = 0.60; P less than 0.01) and to plasma urea (r = 0.36; P = 0.06). In contrast, leu-enkephalin was suppressed in uraemic patients (P less than 0.001). Met-enkephalin fell slightly but significantly (P less than 0.02) after both haemodialysis and haemofiltration; however, on average it remained at concentrations four times higher than normal. No changes in plasma leu-enkephalin were observed after haemodialysis and haemofiltration. The cause(s) of the altered plasma concentrations of these opioid substances remains to be clarified.
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PMID:Plasma met-enkephalin and leu-enkephalin in chronic renal failure. 311 Jun 77

The urinary excretion rates of free cortisol and cortisone as well as of their 20-dihydroisomers have been studied in normal subjects under different physiological or pharmacological conditions. For the estimation of steroid excretion rates, a fully automated, liquid-chromatographic method was used. In normal subjects, the median steroid excretion rates of free cortisol, cortisone, 20-alpha-dihydrocortisol, 20-beta-dihydrocortisol, 20-alpha-dihydrocortisone and 20-beta-dihydrocortisone were 6.7, 8.0, 9.8, 5.2, 5.7 and 1.3 mumol/mol creatinine. The excretion rates measured at three different intervals of the day followed a circadian rhythm similar to that known for the cortisol secreting activity of the adrenal gland. After adrenal stimulation by i.v. application of 250 micrograms of tetracosactide hexaacetate, (Synacthen, corticotropin beta 1-24) excretion of urinary cortisol was significantly higher than those of the other steroids. During a 24 h infusion of corticotropin beta 1-24, the excretion rates of cortisol and its C-20 reduced isomers increased to a significantly greater extent than those of cortisone and its C-20 reduced isomers. During a four-hour infusion of hydrocortisone, the relative increase of cortisol excretion was greater than that of the other steroids. During a five-hour infusion of metyrapone at different dosages, the excretion of all steroids decreased in a dose-dependent manner. The present data indicate that the 20-dihydroisomers of cortisol and cortisone in human urine primarily originate from the peripheral metabolism of cortisol rather than from adrenal secretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:20-Dihydroisomers of cortisol and cortisone in human urine: excretion rates under different physiological conditions. 362 32

1. The blood pressure, renal and metabolic effects of adrenocorticotropic hormone (ACTH) have been studied in six normotensive subjects and two patients with Addison's disease on maintenance steroid therapy. 2. In normotensive subjects, 5 days ACTH treatment (0.5 mg 12 hourly) was associated with a rise in systolic blood pressure and mean arterial pressure. There was a small rise in diastolic pressure but no consistent change in heart rate. Plasma sodium increased and plasma potassium fell. Serum creatinine and urea concentrations were unchanged. Fluid intake increased and urine output was unchanged but ACTH withdrawal was associated with a diuresis. There was an initial reduction in urinary sodium excretion and a natriuresis after ACTH withdrawal. Plasma volume and body weight rose. 3. ACTH produced increases in plasma cortisol, 11-deoxycortisol, corticosterone, deoxycorticosterone, aldosterone, 17 alpha-hydroxyprogesterone and 17 alpha,20 alpha-dihydroxyprogesterone. Plasma renin concentration fell. 4. Patients with Addison's disease showed no change in blood pressure or in any other metabolic variable studied. 5. The effects of ACTH in man resembled those found in sheep.
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PMID:Blood pressure, renal and metabolic effects of ACTH in normotensive man. 627 70


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