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)

After burn trauma, a very marked endocrine response occurs. Almost all the known hormones take part in it. Their response influences very much the postburn metabolic changes and participates in the integration of the body's response with the nervous and immune systems. In this review, mainly the changes in various hormone levels are described, as well as the possible role of the acute phase response after burn trauma, and the communications between the endocrine and immune systems, the cells of the latter are able to respond to various hormonal stimuli and to secrete various hormones themselves. Some of the hormones are very sensitive indicators of the burn stress, e.g., the T3 levels (very low), testosterone in males (very low), dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEA-S) (very low), ADH, catecholamines, renin and angiotensin II, cortisol (high), 17-beta-estradiol in males (usually elevated). Other hormones are usually elevated, but not always (ACTH, aldosterone, prolactin, glucagon, immunoreactive insulin, beta-endorphin, rT3, 11-beta-hydroxyandrostenedione), but there are hormones that are unually low (T4, FSH, androstenedione, progesterone--the latter especially in females). Calcitonin, parathyroid hormone, growth hormone are sometimes elevated, as well as LH (measured with RIA methods). TSH is usually normal, the biologically measured LH was reported to be low. The levels of the sensitive indicators of burn stress may be used to evaluate the effect of treatment: if the burn patient is properly treated, the indicators may become earlier normal.
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PMID:Endocrine changes after burn trauma--a review. 251 73

To assess the effect of continuous heat exposure on the nocturnal patterns of renin, aldosterone, adrenocorticotropic hormone (ACTH), and cortisol, six young men were exposed to thermoneutral environment for 5 days, followed by a 5-day acclimation period in a hot dry environment (35 degrees C). Blood was collected at 10-min intervals during the second night at thermoneutrality (N0) and during the first (N1) and the last (N5) nights of heat exposure. Polygraphic recordings of sleep were scored according to established criteria. Continuous heat exposure led to progressive decreases in the 24-h urinary volume and in Na excretion, whereas urinary osmolality increased. After 5 days of uninterrupted heat, significant increases were found in plasma volume (P less than 0.05), osmolality (P less than 0.01), plasma Na (P less than 0.01), and protein levels (P less than 0.05). Sweat gland output increased during the first 3 days and then declined without any concomitant increases in body temperature. Compared with N0, there were no differences in plasma renin activity (PRA) and aldosterone (PA) profiles during N1 at 35 degrees C. However, during N5 the mean PRA and PA levels were significantly (P less than 0.05) enhanced, and their nocturnal oscillations were amplified (P less than 0.05). This amplification occurred mainly in the second part of the night when regular rapid-eye-movement and non-rapid-eye-movement sleep cycles were observed, leading to a general upward trend in the nocturnal profiles. The relationship between the nocturnal PRA oscillations and the sleep cycles was not modified. ACTH and cortisol patterns were not affected by continuous heat exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Amplification of nocturnal oscillations in PRA and aldosterone during continuous heat exposure. 254 Jan 45

Systemic hypoxia has been reported to inhibit selectively aldosterone secretion in vivo. The mechanism of this inhibition has not been elucidated. We hypothesized that decreased tissue PO2 directly inhibited aldosteronogenesis. To test this hypothesis, we exposed dispersed adrenocortical cells (90% glomerulosa/10% fasciculata) to decreased PO2 in vitro while simultaneously stimulating aldosterone secretion with angiotensin II, N6,2'-O-dibutyryladenosine 3',5'-cyclic monophosphate (dibutyryl cAMP) adrenocorticotropic hormone (ACTH)-(1-24), or progesterone. Decreasing buffer PO2 from approximately 150 to approximately 85 Torr significantly inhibited basal and angiotensin II, cAMP, progesterone, and ACTH-stimulated aldosterone secretion at all doses of secretagogue. Inhibition was largest for angiotensin II (55 +/- 9% inhibition at 1 microM) and cAMP (54 +/- 8% at 3 mM) and lowest for ACTH (24% at 100 nM) and basal aldosterone secretion (31 +/- 7%). This inhibition was reversed by returning the buffer PO2 to 150 Torr. Cortisol secretion was not significantly inhibited by decreased buffer PO2. We conclude that decreased buffer PO2 significantly inhibits aldosterone secretion in vitro, and this inhibition is reversible and specific. Hypoxia-induced inhibition of aldosterone secretion in vivo may be caused, at least in part, by a direct effect of low tissue PO2 within the adrenal cortex.
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PMID:Low oxygen selectively inhibits aldosterone secretion from bovine adrenocortical cells in vitro. 254 24

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

We have reported that infusion of atrial natriuretic factor (ANF) inhibited the rise in plasma renin activity (PRA) in response to constriction of the abdominal aorta to cause a reduction in renal perfusion pressure (RPP). To evaluate the effect of ANF on neural control of renin release, acute thoracic inferior vena caval constriction (TIVCC) was performed in conscious dogs to reduce arterial pressure by 25% of control and stimulate PRA by a reflex increase in renal nerve activity and a reduction in RPP. Propranolol was used to block neural stimulation of renin release. TIVCC caused significant increases in PRA, plasma aldosterone, arginine vasopressin (AVP), and adrenocorticotropic hormone (ACTH) concentrations. The increase in PRA was significantly reduced by the infusion of either ANF at 20 ng.kg-1.min-1 or propranolol. The combined infusion of ANF and propranolol produced an additive and complete inhibition of the renin response to TIVCC; therefore the effect of ANF is independent of neural stimulation of renin release. ANF at 20 ng.kg-1.min-1 also inhibited increases in aldosterone, AVP, and ACTH, but ANF at 5 ng.kg-1.min-1 only affected the aldosterone response to TIVCC. Therefore ANF inhibits angiotensin II-stimulated aldosterone synthesis and/or secretion at very low doses and at higher doses attenuates reflex increases in AVP and ACTH caused by hypotension.
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PMID:Mechanism of inhibition of renin response to hypotension by atrial natriuretic factor. 254 56

Rat adrenal glomerulosa cells labelled for 18 h with [3H]inositol responded to angiotensin II with a dose-dependent stimulation of the accumulation of inositol monophosphate, inositol bisphosphate and inositol trisphosphate. Addition of adrenocorticotropic hormone (ACTH) (10(-7)M) reduced the maximum responses without altering the EC50 values for angiotensin II. Thus, ACTH acted as a non-competitive inhibitor with respect to angiotensin II. No inhibition was observed in cells labelled for 2 h with [3H]inositol. Detailed examination of the inhibition showed that ACTH(1-24) was the most potent inhibitor, with ACTH(1-39) being 10-fold less potent. A mixture of alpha-melanocyte-stimulating hormone (alpha-MSH) (ACTH(1-13] and corticotropin-like intermediate lobe peptide (ACTH(18-39] was similarly inactive. ACTH(5-24) did not produce detectable inhibition. In terms of specificity, the receptor mediating ACTH inhibition of phosphatidylinositol turnover was similar to the receptor which mediated stimulation of aldosterone synthesis. Inhibition by ACTH was additive with inhibition produced by dibutyryl cAMP demonstrating that it was not mediated by rises in intracellular cAMP. ACTH inhibition also was additive with inhibition by the calcium channel blocker, nifedipine. These results demonstrate an interaction between ACTH receptors and angiotensin II receptors in adrenal glomerulosa cells at the level of their receptor-second messenger pathways.
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PMID:Adrenocorticotropic hormone inhibits angiotensin II-stimulated inositol phosphate accumulation in rat adrenal glomerulosa cells. 254 42

The responses of human adrenocortical cells to stimulation by ACTH(1-24), desacetyl-alpha-MSH, alpha-MSH and angiotensin II amide have been compared. Both desacetyl-alpha-MSH, thought to be the major form of the peptide in the human pituitary and in circulating plasma, and alpha-MSH caused a significant stimulation of aldosterone, corticosterone and cortisol secretion. Significant stimulation of the production of these steroids was obtained with desacetyl-alpha-MSH at a concentration of 1 nmol/l, while the response to alpha-MSH was considerably less sensitive, with a minimum effective concentration of 0.1 mumol/l. These values compared with minimum effective concentrations of 1 pmol/l for ACTH and 0.1 mumol/l for angiotensin II amide. Although cell types were not separated, it is possible to conclude that none of the peptides showed any specificity for the zona glomerulosa, and in each case the same minimum effective concentration of peptide was required for both aldosterone and cortisol secretion. Yields of steroid obtained under conditions of maximal stimulation by ACTH(1-24), alpha-MSH and desacetyl-alpha-MSH were at least three to five times the basal output of aldosterone, four to eight times that for corticosterone and more than seven to sixteen times that for cortisol. Angiotensin II amide was a relatively poor stimulant with maximal stimulation only 1.5 x basal. In these experiments the minimum effective concentration for desacetyl-alpha-MSH (1 nmol/l) was close to the circulating concentration of desacetyl-alpha-MSH (0.3 nmol/l) in man, and it is thus possible that this peptide may have a physiological role in the control of adrenocortical function.
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PMID:Actions of desacetyl-alpha-melanocyte-stimulating hormone on human adrenocortical cells. 254 12

To investigate possible abnormalities of the hypothalamic-pituitary axis in patients with chronic renal failure on dialysis, we have examined the effects of insulin-induced hypoglycemia on the adrenal steroid responses. In normal subjects, plasma aldosterone and cortisol concentrations increase significantly in response to hypoglycemia, with good correlation. In the patients with end-stage renal disease (ESRD) however, insulin-induced hypoglycemia fails to elicit significant increases in the plasma cortisol and aldosterone levels. To test the adrenal responsiveness to adrenocorticotropin (ACTH), we administered ACTH to both groups. Plasma cortisol and aldosterone responses are similar in both groups suggesting that the adrenal responsiveness to ACTH is not impaired. We also investigated the responsiveness of the renin-angiotensin-aldosterone system in response to volume contraction by hemofiltration in patients with ESRD. Neither plasma renin activity nor plasma aldosterone concentration change significantly following such contrived volume contraction. These results reveal several endocrinologic abnormalities in the patients with ESRD on chronic hemodialysis.
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PMID:Aldosterone response to insulin-induced hypoglycemia in hemodialysis patients. 254 16

Aldosterone is a major regulator of fluid and electrolyte balance after hemorrhage and is released from the adrenal cortex by the action of adrenocorticotropin (ACTH) and angiotensin II (AII). Past work has shown that the hemorrhage-induced release of ACTH and cortisol is potentiated by prior hemorrhage. We therefore studied the response of adrenal aldosterone secretion to repeated hemorrhage and its control by ACTH and AII. Six awake dogs with chronic lumboadrenal vein catheters were bled 10% of measured blood volume (H1) with reinfusion at 30 minutes. The hemorrhage was repeated 5 hours later (H2). Adrenal presentation rates for AII (AII-PR) and ACTH (ACTH-PR) were calculated for each sample. Control hormonal and hemodynamic parameters before each hemorrhage were not different; hemodynamic responses to H1 and H2 did not differ. Aldosterone secretion increased significantly after each hemorrhage. The increase in aldosterone secretion after H1 was associated with an early increase in AII-PR and late increase in ACTH-PR. Aldosterone secretion following H2 was greater than that following H1 and was associated with early and larger responses of AII-PR and ACTH-PR. Aldosterone secretion following H1 correlated with the AII-PR (r = 0.75; p less than 0.001), but not with the ACTH-PR. In contrast, aldosterone secretion following H2 correlated with both the AII-PR (r = 0.54; p less than 0.01) and ACTH-PR (r = 0.71; p less than 0.001) and multiple regression analysis showed a highly significant relation with both AII and ACTH (r = 0.81; p less than 0.001). The data suggest that aldosterone secretion after initial small hemorrhage occurs as a result of increased AII, whereas both AII and ACTH may contribute to the larger aldosterone secretory response to H2. Since major trauma commonly involves at least two insults separated in time (e.g., injury followed by surgery), potentiated responses of aldosterone and other pituitary-adrenal hormones (ACTH, vasopressin, and cortisol) may have important implications for the control of fluid and electrolyte balance and metabolism in injured patients.
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PMID:Aldosterone secretion following non-hypotensive hemorrhage is potentiated by prior blood loss. 254 67

An effect of enalapril maleate on the activity of renin-angiotensin-aldosterone system and sympathetic reactivity, erythrocyte prostaglandin and sodium levels as well as blood beta-endorphin was investigated in 28 patients with the essential arterial blood hypertension. It was found that enalapril maleate significantly increased plasma renin activity, decreased plasma norepinephrine and its 24-hour excretion, and decreased erythrocyte beta-endorphin and sodium levels. Blood epinephrine and aldosterone levels and their daily excretion remained unchanged similarly to prostaglandins. The above results suggest that a decrease in sympathetic system activity and intracellular sodium concentration may play a role in the hypotensive action of enalapril maleate related to the inhibition of angiotensin II formation.
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PMID:[Effect of treatment with enalapril maleate on the levels of circulating catecholamines, beta endorphins, prostaglandins, and concentration of sodium in erythrocytes in patients with essential hypertension]. 255 61


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