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)

To evaluate to what extent opioid secretion in exercise induces the release of atrial natriuretic factor (ANF), six healthy male volunteers who were trained subjects, were submitted to two maximal exercise tests with and without (control) opioid receptor blockade by Naltrexone. Blood samples were drawn before (rest) and after exercise (post-exercise) in order to measure human ANF (alpha h ANF), beta-endorphin, plasma aldosterone concentration (PAC) plasma renin activity (PRA) and adreno-cortico trophic hormone (ATCH) by radio-immunological methods. Expired gas was collected during exercise to measure oxygen consumption. On average, the same maximal oxygen consumption (VO2max) during exercise was reached by all subjects with and without treatment. Plasma ANF level at rest slightly decreased after administration of Naltrexone; the response to physical exercise was significantly reduced by Naltrexone. There was no statistical difference between plasma levels of beta-endorphin, PRA and ACTH at rest nor in the post-exercise situation under the influence of Naltrexone. The PAC increased significantly at rest after Naltrexone administration but there was no statistical difference between both values after exercise. These data demonstrate that: (1) ANF secretion during exercise is influenced by the level of beta-endorphin in the plasma; (2) the possible inhibitory role of ANF on aldosterone secretion during exercise is probably over-ruled by the increase in plasma ACTH and PRA.
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PMID:Influence of endogenous opioids on atrial natriuretic factor release during exercise in man. 255 88

Since the intracellular messengers of various proopiomelanocortin-derived peptides remain ambiguous at best, we have investigated the possible involvement of phosphoinositide metabolism in aldosterone secretion evoked by alpha-MSH, beta-LPH, as well as ACTH in rat and calf adrenal glomerulosa cells. We have also examined the cAMP responses in the adrenal glomerulosa cells to alpha-MSH comparing it with those of ACTH. Our results showed that neither alpha-MSH, beta-LPH, nor ACTH increased inositol triphosphate (IP3) or other inositol phosphates in adrenal glomerulosa cells while increasing aldosterone secretion from the same cells. Angiotensin II, known to cause hydrolysis of the phosphoinositides, increased IP3 in these adrenal cells in a dose-dependent manner. Both ACTH and alpha-MSH raised the cAMP levels in the calf adrenal glomerulosa cells, although the magnitude of the increase of cAMP in response to ACTH was greater. These findings suggest that IP3 as a mediator of alpha-MSH- and beta-LPH-induced aldosterone secretion is not likely and other mediator(s) may be involved.
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PMID:Proopiomelanocortin-derived peptides, phosphoinositides, cAMP, and aldosterone secretion. 255 49

It was been shown that physical exercise increases plasma atrial natriuretic peptide (ANP) level. This effect was attributed to the hemodynamic changes of exercise which could increase atrial volume and result in ANP secretion. On the other hand, it was evidenced that morphine and opiate peptides greatly stimulate ANP release. To evaluate to what extent the endogenous opioid secretion during exercise induces the ANP release, six healthy volunteers male trained subjects were submitted to two maximal exercise tests with and without (placebo) opiate receptors blockade by naltrexone (50 mg per os). Blood samples were drawn before (rest) and after maximal exercise in order to measure by radioimmunological methods human atrial natriuretic peptide (alpha-h-ANP), beta-endorphin, plasma aldosterone (ALD), plasma renin activity (PRA) and corticotrophin (ACTH). Expired gas was collected during exercise to measure oxygen consumption. Subjects reached the same value of maximal oxygen consumption (VO2 max) at the end of exercise whatever treatment. Plasma ANP level at rest decreases slightly after administration of naltrexone (32.8 +/- 6.3 pg/ml with placebo versus 21.3 +/- 4.6 pg/ml with naltrexone) but the response to physical exercise was significantly reduced by naltrexone (73.3 +/- 14.9 pg/ml with placebo versus 46.9 +/- 8.6 pg/ml with naltrexone) (p less than 0.05). There was no statistical difference according to the treatment between the plasma levels of beta-endorphin, PRA and ACTH at rest as well as at the end of a maximal exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Atrial natriuretic peptide response to physical exercise is inhibited by an antagonist of the opioid receptors]. 256 Oct 15

When the dose-response curve of adrenocorticotropin (ACTH)-induced aldosterone secretion is compared to that of ACTH-induced intracellular cAMP, the ED50 for intracellular cAMP is more than 10 times as high as that for aldosterone production. In contrast, the dose-response curve of forskolin-induced aldosterone secretion correlates well with that for forskolin-induced intracellular cAMP. ACTH, but not forskolin, increases calcium influx into glomerulosa cells without inducing the mobilization of calcium from an intracellular pool. The effect of ACTH on calcium influx is dose-dependent and ED50 is 3.5 X 10(-11) M. In a perifusion system, the effect of 1 nM ACTH on aldosterone secretion is much greater than that of 1 microM forskolin, even though these two stimulators induce identical increases in the intracellular cAMP. Perifusion with combined A23187 (50 nM) and forskolin (1 microM) stimulates aldosterone secretion to a value comparable to that induced by 1 nM ACTH. Likewise, BAY K 8644 (1 nM), which induces a comparable increase in calcium influx, potentiates the effect of 1 microM forskolin. When the intracellular [Ca2+] is fixed at either 100 or 300 nM, forskolin-stimulated intracellular cAMP content is identical, but ACTH-stimulated intracellular cAMP content at 100 nM [Ca2+]i is 60% of that at 300 nM [Ca2+]i. Both the ACTH- and forskolin-induced aldosterone secretion rate is higher at 300 nM than at 100 nM [Ca2+]i. These results indicate that ACTH stimulates calcium influx, that calcium potentiates ACTH-induced but not forskolin-induced cAMP generation, and that Ca2+ and cAMP act as synarchic messengers in ACTH-mediated aldosterone secretion.
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PMID:Role of calcium and cAMP in the action of adrenocorticotropin on aldosterone secretion. 257 47

We investigated the effects of sevoflurane anesthesia and of surgery, on the endocrine functions as reflected by plasma levels of cortisol, aldosterone, ACTH, beta-endorphin-like immunoreactivity, prolactin, insulin, growth hormone, glucagon and glucose in surgical patients.
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PMID:Endocrine evaluation of sevoflurane, a new inhalation anesthetic agent. 262 72

In humans, the syndrome of cortisol resistance is characterized by the absence of signs and symptoms of Cushing's syndrome, elevated total and unbound plasma cortisol concentrations, and increases in urinary free cortisol excretion and plasma adrenocorticotropic hormone. In one family, a severely affected member had hypertension and hypokalemic alkalosis associated with increased plasma concentrations of corticosterone and deoxycorticosterone. These patients are resistant to suppression of the pituitary-adrenal axis by dexamethasone. Dexamethasone therapy, however, effectively corrected hypertension and hypokalemic alkalosis in the severely affected patient, without causing signs of glucocorticoid excess. The glucocorticoid receptor from these patients has a low affinity for glucocorticoids and is unstable during thermal activation. Both the molecular weight of the glucocorticoid receptor and the size of the corresponding mRNA are similar to those of normal controls. Transformation of B-lymphocytes with Epstein-Barr virus leads to induction of glucocorticoid receptors. Receptor induction, however, is lower in patient cells than those obtained from normal controls. This decreased induction parallels decreased expression of glucocorticoid receptor mRNA. Thus, in this form of glucocorticoid resistance the glucocorticoid receptor is abnormal and leads to diminished target organ responsiveness. Many New World primates exhibit glucocorticoid "resistance," without apparent pathology. These species have markedly elevated plasma cortisol, both total and unbound concentrations, increased urinary free cortisol excretion, and marked increases in plasma adrenocorticotropic hormone and beta-endorphin. The glucocorticoid receptors of these primates have decreased affinity for glucocorticoids, are thermolabile, and are not induced by Epstein-Barr virus transformation as indicated by specific binding and mRNA expression. Both the molecular weight of the glucocorticoid receptor and the size of the corresponding mRNA are similar to those of normal controls. Despite the high plasma cortisol concentrations in these primates, there is no sodium retention and aldosterone levels are actually increased. The kidney aldosterone receptor cross-reacts poorly with cortisol, explaining the absence of sodium retention. New World primates also have progesterone, estrogen, aldosterone, and vitamin D insensitivity, suggesting a common factor linking steroid hormone receptors.
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PMID:Glucocorticoid resistance in humans and nonhuman primates. 264 36

Changes in blood insulin, thyroxine, triiodothyronine, thyrotropin, somatotropin, corticotropin, cortisol, and aldosterone were defined in 46 male patients with coronary heart disease during daily graded exercises performed on a bicycle ergometer for 30 days. The exercises led to improvement of health in 44 patients. There was a significant reduction in baseline insulin and aldosterone levels and a tendency to lower corticotropin and triiodothyronine concentrations. The amounts of somatotropin, thyrotropin, thyroxine, and cortisol failed to greatly change during the exercise.
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PMID:[Changes in the hormonal profile in patients with ischemic heart disease during physical training]. 269 93

Experiments on rats have shown that the dopamine agonist parlodel produces a noticeable inhibitory effect on function of the pituitary-adrenal system by a decrease in corticotropin secretion and direct influence on aldosterone synthesis and secretion. Changes in corticosterone level caused by parlodel are related to ACTH action and inhibition of activity of the microcirculatory bed of the adrenal fascicular zone. The dopamine agonist parlodel produces no effect on metabolism of the steroid hormones: corticosterone and testosterone in the rat hepatic tissue.
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PMID:[Effect of the dopamine agonist parlodel on steroid hormone secretion and their metabolism in the liver]. 282 35

The role of angiotensin II in the hormonal and renal responses to maximal exercise was investigated by using the angiotensin-converting enzyme inhibitor captopril. Nine male subjects performed a standardized maximal treadmill test with and without acute captopril treatment (25 mg orally). At rest, captopril elevated plasma renin activity and lowered aldosterone levels. With maximal exercise, captopril treatment reduced the increase in mean arterial blood pressure by 8 mmHg and the increase in plasma renin activity by 3.0 ng ANG I.ml-1.h-1. The responses of adrenocorticotropin (ACTH), cortisol, and vasopressin to maximal exercise were not altered by captopril treatment. Although aldosterone levels were reduced at rest with captopril, during maximal exercise no difference was noted between treatments. Captopril treatment had no effects on the renal handling of salts or water during exercise. In conclusion, angiotensin II plays a role in the increase in mean blood pressure during maximal exercise in normal subjects but has no effect on the exercise responses of ACTH, vasopressin, and aldosterone or on the renal handling of salts and water.
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PMID:Hormonal and renal responses to converting enzyme inhibition during maximal exercise. 282 83

Aldosterone secretion from adrenal glomerulosa cells can be stimulated by angiotensin II (AII), extracellular potassium and adrenocorticotropin (ACTH). Since the mitochondria can recognize factors generated by AII (cyclic-AMP-independent) and ACTH (cyclic AMP dependent), it is reasonable to postulate the existence of a common intermediate in spite of a different signal transduction mechanism. We have evaluated this hypothesis by stimulation of mitochondria from glomerulosa gland with fractions isolated from glomerulosa gland stimulated with AII or from fasciculata gland stimulated with ACTH; the same fractions were tested using mitochondria from fasciculata cells. Postmitochondrial fractions (PMTS) obtained after incubation of adrenal zona glomerulosa with or without AII (10(-7) M) or ACTH (10(-10) M), were able to increase net progesterone synthesis 5-fold in mitochondria isolated from non-stimulated rat zona glomerulosa. In addition, AII in zona glomerulosa produced in vitro steroidogenic fractions that were able to stimulate mitochondria from zona fasciculata cells. Inhibitors of arachidonic acid release and metabolism blocked corticosterone production in fasciculata cells stimulated with ACTH. This concept is supported by the experiment in which bromophenacylbromide and nordihydroguaiaretic acid also blocked the formation of an activated PMTS. In fact, non-activated PMTS, in the presence of exogenous arachidonic acid AA, behaved as an activated PMTS from ACTH stimulated cells. We suggest that the mechanisms of action of ACTH and AII involve an increase in the release of AA and an activation of the enzyme system which converts AA in leukotriene products.
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PMID:Leukotrienes as common intermediates in the cyclic AMP dependent and independent pathways in adrenal steroidogenesis. 282 7


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