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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epinephrine (E) and norepinephrine (NE) levels were measured simultaneously in the adrenal veins of 6 patients before and after stimulation with 0.25 mg beta 1-24 ACTH. In 1 patient with Cushing's syndrome, E and NE were also measured before and 30 min after dexamethasone. There was a significant increase in NE and E secretion (p less than 0.002) from both adrenal glands after ACTH stimulation. In the patient with Cushing's syndrome, there was also a slight increase in plasma E levels after dexamethasone. It is postulated that ACTH stimulated NE and E secretion by augmenting blood flow through the adrenals and by induction of tyrosine hydroxylase and dopamine beta-hydroxylase, although a direct effect of ACTH on NE and E secretion cannot be excluded. It is also possible that the increase in adrenal catecholamine secretion after ACTH may be due to ACTH augmentation of catecholamine secretion by endogenous opioids such as beta-endorphin.
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PMID:ACTH stimulation of adrenal epinephrine and norepinephrine release. 300 Sep 12

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

The reliability of the beta 1-24 corticotropin test, which is both cheap and safe, in the assessment of the hypothalamic-pituitary-adrenocortical function was re-evaluated by comparing its results with those of the metyrapone test in 71 subjects: 30 controls and 51 patients with suspected pituitary-adrenal dysfunction. Response to a 500 micrograms intramuscular injection of beta 1-24 corticotropin was evaluated by measuring the 60 min plasma cortisol levels; 4.5 g of metyrapone divided into 6 doses were then administered orally and response was evaluated by measuring plasma 11-desoxycortisol levels. A highly significant correlation (r = 0.79; p less than 0.001) was observed between plasma cortisol and plasma 11-desoxycortisol levels. The results were best interpreted by expressing the values obtained as plasma cortisol concentrations which, in normal subjects are at least 21 micrograms/100 ml. The rapid beta 1-24 corticotropin test was found to be very reliable (sensitivity 90%, specificity 100%) to detect adrenal insufficiency, irrespective of the organs affected on the hypothalamic-adrenocortical axis.
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PMID:[Rapid beta 1-24-corticotropin test in the exploration of the corticotropic axis. 71 cases]. 609 44

Primary cultures of neonatal murine brain have been reported to express multiple receptors that regulate adenylate cyclase activity. Since for the most part these results were obtained with mixed cell cultures, it has been difficult to define receptor profiles for specific cell types. With this concern in mind a series of studies has been initiated designed to identify specific receptors present on highly purified, immunocytochemically defined astroglia derived from the cerebral cortices of neonatal rats. In this study the capacity of a variety of peptide hormones to regulate cyclic AMP metabolism in these cells was examined. Fibroblasts derived from the meninges represent a predictable source of contamination in primary CNS culture. Thus, to assign more clearly specific receptors to the astroglial cell population, receptor-mediated regulation of cyclic AMP accumulation was also examined in fibroblasts. Cyclic AMP accumulation in astroglia was stimulated by catecholamines (acting at beta 1-adrenergic receptors), prostaglandin E1, vasoactive intestinal polypeptide, alpha-melanocyte-stimulating hormone, and adrenocorticotropin. Bombesin, luteinizing hormone-releasing hormone, neurotensin, thyrotropin-releasing hormone, somatostatin, secretin, and vasopressin did not significantly increase cyclic AMP levels in these cultures. Catecholamines, acting at alpha 2-adrenergic receptors, and somatostatin inhibited agonist-stimulated cyclic AMP accumulation. In meningeal cell cultures catecholamines (acting at beta 2- and alpha 2-adrenergic receptors) and prostaglandin E1 regulated cyclic AMP levels. However, vasoactive intestinal peptide did not stimulate and somatostatin did not inhibit cyclic AMP accumulation in these cells.
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PMID:Regulation of cyclic AMP accumulation by peptide hormone receptors in immunocytochemically defined astroglial cells. 620 41

The lipid mobilizing effects of corticotropin (ACTH), beta 1-24-corticotropin-tetracosactide (TCA) and isoprenaline (ISO) were studied in parallel experiments in older rabbits (six months, weight 3.5 kg) and rats (age 75-85 days, weight 275 g) in vitro. The results were analysed quantitatively. Compared with the effect in younger rats the lipid mobilizing action of ISO in older animals does not differ. The same applies to the very low ISO lipolytic potency in rabbits. The ACTH intrinsic activity and affinity decrease in aging rabbits, but not in aging rats. At the concentration 1 x 10(-9) mol/l of TCA 35% of its maximum effect is reached in rabbits and almost the maximum in rats. In comparison with the maximum response to ACTH the maximum of TCA is two times higher in rabbits whereas in rats it reaches only 80% of the ACTH maximum. The order of the intrinsic activities is in older rats and rabbits different: ISO much greater than ACTH greater than TCA (1.00:0.81:0.64) in rats and TCA greater than ACTH greater than ISO (1.00:0.53:0.31) in rabbits. The affinity relations TCA greater than ISO greater than ACTH are identical in both species with the ratios of ACTH:ISO:TCA = 1:50:1740 in rats and 1:34:915 in rabbits. TCA exerts the strongest lipolytic potency in rats which is 5.5 times greater than in rabbits. On the contrary the intrinsic activity of TCA in rabbits is the highest. In older rabbits the ACTH adipokinetic intrinsic activity and affinity decrease faster than those in ISO. The species differences especially in relation to ISO also remain preserved in older animals and this applies to the TCA lipolytic effects, which in turn do not seem to change with aging as much as the effects of ACTH. When evaluating the species differences or the sensitivity changes connected with aging in the action of lipolytic drugs, the intrinsic activity and affinity should be considered separately.
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PMID:Quantitative analysis of the lipid-mobilizing effects of corticotropin, beta 1-24--corticotropin (tetracosactide) and isoprenaline in older rats and rabbits. 626 29

Changes of cyclic AMP levels were used to assess the specificity of the beta-adrenergic receptor in primary cultures of cells prepared from the intermediate lobe of rat pituitary gland. During a 4 min incubation, beta-adrenergic agonists led to a 4 to 6 fold stimulation of cyclic AMP concentration with the following order of potency (Kd values): zinterol (0.75 nM) greater than hydroxybenzylisoproterenol (1.0 nM) greater than (--)-isoproterenol (4.6 nM) greater than soterenol greater than (7.7 nM) greater than (--)-epinephrine (10 nM) greater than OPC 2009 (procaterol, 11 nM) much greater than (--)-norepinephrine (300 nM). The potent antagonists cyanopindolol, (--)-propranolol and hydroxybenzylpindolol reversed the stimulatory effect of (--)-isoproterenol at Kd values of 0.4-0.6 nM. Other beta-adrenergic antagonists had the following order of potency: pindolol = (--)-alprenolol = timolol (0.9-1.0 mM) much greater than metoprolol (100 nM) greater than dichloroisoproterenol (300 nM) greater than butoxamine (1100 nM). The beta 1-selective antagonist practolol had a low potency at 700 nM. The stereoselectivity of the receptor is indicated by the 400 to 70 fold higher potency of the (--)-isomers of isoproterenol, epinephrine and propranolol as compared to their (+)-stereoisomers. The data show that the beta-adrenergic receptor in the intermediate lobe of the rat pituitary gland is mainly of the bet 2-subtype. Study of this pure population of postsynaptic beta-adrenergic receptors where binding could be correlated with other parameters of cellular activity (cyclic AMP formation and alpha-MSH secretion) should yield useful information about the less accessible adrenergic systems of the brain.
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PMID:Specificity of the beta 2-adrenergic receptor stimulating cyclic AMP accumulation in the intermediate lobe of rat pituitary gland. 628 11

AtT-20 cells comprise a mouse anterior pituitary tumor cell line that synthesizes and secretes adrenocorticotropin hormone (ACTH). beta-Adrenergic receptors were characterized on AtT-20 cells using receptor binding methodology and the ability of beta-receptor agonists to stimulate intracellular cyclic adenosine 3':5'-monophosphate (cAMP) formation and the release of ACTH immunoreactivity. The density of beta-receptors on membrane preparations of these cells is 64 fmol/mg of protein and their affinity constant (KD value) for tritiated dihydroalprenolol is 11 nM. The binding of [3H] dihydroalprenolol to AtT-20 cells is stereoselectively inhibited by propranolol and isoproterenol but is not affected by phentolamine. The beta-receptors on these cells appear to be of the beta 2-receptor subtype since a selective beta 2-receptor agonist, salmefamol, can inhibit [3H]dihydroalprenolol binding, whereas practolol, a beta 1-receptor blocker, is ineffective. (-)-Isoproterenol stimulates cAMP formation in AtT-20 cells and this effect is blocked by dl-propranolol. Both l-epinephrine and l-norepinephrine induce dose-dependent increases in cAMP formation with the former agonist being more potent. Salmefamol also stimulates cAMP formation in these cells. The secretion of ACTH from AtT-20 cells is induced by (-)-isoproterenol as well as by other adrenergic agonists. The isoproterenol effect on ACTH release is stereoselective, calcium dependent, and blocked by dl-propranolol but not by phentolamine or practolol.
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PMID:Activation of beta 2-adrenergic receptors on mouse anterior pituitary tumor cells increases cyclic adenosine 3':5'-monophosphate synthesis and adrenocorticotropin release. 630 Mar 55

Previous work in our laboratory has shown that stimulation of beta 2-adrenergic receptors on mouse anterior pituitary tumor cells causes the secretion of immunoreactive adrenocorticotropin (ACTH). The present study was designed to test the hypothesis that catecholamines can cause the release of ACTH in vivo by the direct stimulation of beta 2-adrenergic receptors in the rat anterior pituitary. Systemic administration of a beta-adrenergic receptor agonist (-)-isoproterenol resulted in an increase in plasma ACTH levels in intact animals and in rats with transected pituitary stalks. This effect could be blocked by the beta-adrenergic receptor antagonist, propranolol, but not by the specific beta 1-adrenergic receptor antagonist, practolol. Salmefamol, a beta 2-adrenergic receptor agonist also elevated plasma ACTH levels in stalk-sectioned animals. Dexamethasone, a glucocorticoid that inhibits the synthesis and release of ACTH from the anterior pituitary but not the intermediate lobe, prevented the elevation of ACTH secretion by (-)-isoproterenol in stalk-transected rats. These data indicate that beta 2-adrenergic receptors are present on anterior pituitary cells and suggest that catecholamines can directly stimulate ACTH secretion.
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PMID:Direct stimulation of beta 2-adrenergic receptors in rat anterior pituitary induces the release of adrenocorticotropin in vivo. 631 39

Administration of ACTH beta 1-24 (0.25 mg, i.m.) in six healthy subjects reduces blood prolactin response to sulpiride (100 mg, i.m.). Dexamethasone (2 mg, orally, given at 11.00 p.m. of preceding day) blocks blood prolactin response to insulin-induced hypoglycemia (0.20 U. kg of "Actrapid" Novo, i.v.) in six voluntary healthy subjects. Intravenous naloxone (0.4 mg/Kg of body weight) blocks in man blood prolactin response to insulin-induced hypoglycemia. On the basis of the above data we can hypothesize that ACTH and dexamethasone have influenced by a feed-back mechanism the lypocorticotropic system. Such system by beta-endorphin release can modulate the secretion of prolactin. Thus inhibition of the lipocorticotropic system may be responsible for the reduced response of the prolactin system to stimulation by sulpiride or hypoglycemic stress.
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PMID:[The lipocorticotropic system and prolactin secretion]. 632 68

In order to explain the differences in the hormone stimulated lipolysis during ontogenic development of rats, the activity of adenylate cyclase was determined in crude plasma membranes of subcutaneous adipocytes of 5, 14, 21 and 45 to 55-day-old animals. Stimulatory effects of nonhormonal and hormonal agents were expressed as the increment in percentage of basal values which were not significantly changed in the age groups studied. The highest stimulatory effect was observed after sodium fluoride in 14 and 21-day-old rats. Guanylylimidodiphosphate and GTP revealed the lowest stimulatory effects in adult animals (greater than 45-day-old). The beta-adrenergic agent isoproterenol revealed the highest stimulatory effect in the 5 and 45-day-old group while in the preparation from 14-day-old rats the adenylate cyclase activity was significantly lower. On the other hand, tetracosactide (beta 1-24-corticotropin) revealed the smallest stimulatory effect on the preparation from 5-day-old rats; its stimulatory effect steadily increased and reached the highest value in adenylate cyclase preparations from adult animals. It can be concluded that the adenylate cyclase system in subcutaneous adipocytes is already basically mature at early ontogenic stages of development in rats. Nevertheless, the explanation for the small variations of the enzyme activity in different age groups requires further study.
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PMID:Adenylate cyclase activity in crude plasma membranes of subcutaneous adipocytes during ontogenetic development of rats. 646 69


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