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)

The responsiveness of lipolysis to the stimulatory agonists noradrenaline, corticotropin and glucagon and to the inhibitory agonists N6-phenylisopropyladenosine, prostaglandin E1 and nicotinic acid was investigated with rat white adipocytes incubated with a high concentration of adenosine deaminase (1 unit/ml). The cells were obtained from fed or 48 h-starved euthyroid animals or from fed or starved animals rendered hypothyroid by 4 weeks of treatment with low-iodine diet and propylthiouracil. Hypothyroidism increased sensitivity to and efficacy of all three inhibitory agonists in their opposition of noradrenaline-stimulated lipolysis. Starvation decreased sensitivity to all three inhibitory agonists when opposing basal lipolysis. Hypothyroidism decreased sensitivity to noradrenaline, glucagon and corticotropin by 37-, 4- and 4-fold respectively and decreased the maximum response to these agonists by approx. 50%, 50% and 75% respectively. Starvation reversed decreases in maximum response to these agonists in hypothyroidism. Starvation in the euthyroid state increased sensitivity to glucagon and noradrenaline, but did not alter sensitivity to corticotropin. Cells from hypothyroid rats were relatively insensitive to Bordetella pertussis toxin, which substantially increased basal lipolysis in the euthyroid state.
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PMID:Sensitivity of adipocyte lipolysis to stimulatory and inhibitory agonists in hypothyroidism and starvation. 302 50

Right medullary and various cardiovascular responses to stimulation of the peripheral end of the splanchnic nerve have been investigated in the presence and absence of exogenous adrenocorticotrophin, ACTH1-24, (5 ng min-1 kg-1). The adrenal-clamp technique was employed in conscious calves, after the pituitary stalk had been cauterized and they had recovered from anaesthesia. The intravenous infusion of ACTH1-24 increased the plasma ACTH concentration by about 1100 pg ml-1 and right adrenal venous output of cortisol by about 400 ng min-1 kg body weight-1. Stimulation of the splanchnic nerve at 4 Hz for 10 min had no effect on either arterial plasma ACTH concentration or the adrenal output of cortisol. Closely similar amounts of both adrenaline and noradrenaline were released in response to nerve stimulation in the presence and absence of exogenous ACTH. In contrast, the fall in adrenal vascular resistance of about 40%, which normally occurred in response to splanchnic nerve stimulation, was completely abolished by ACTH. The adrenal produced relatively large quantities of met-enkephalin-containing peptides. During splanchnic nerve stimulation the output of these increased 2-100-fold, at which time free met5-enkephalin accounted for only 10-20% of total. During ACTH infusion the output of free met5-enkephalin was reduced at rest and during nerve stimulation, but that of total met-enkephalin-containing peptides was unaffected. These results indicate that ACTH or an adrenal steroid may alter the processing of proenkephalin in the adrenal medulla acutely but not total opiate secretion. Alternatively, the presence of ACTH could act by influencing the population of chromaffin cells activated by splanchnic nerve stimulation.
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PMID:Effects of synthetic adrenocorticotrophin on adrenal medullary responses to splanchnic nerve stimulation in conscious calves. 303 Dec 82

Immunoreactive delta sleep-inducing peptide (DSIP) is known to occur in the central nervous system and in body fluids including cerebrospinal fluid, blood and urine. However, the exact nature of the immunoreactive material demonstrated has been a matter of discussion. In the present study, DSIP-like immunoreactivity was demonstrated in the porcine pituitary and adrenal medulla using radioimmunoassay and immunocytochemistry. In the pituitary, the DSIP-like material was present in a subpopulation of the cells storing adrenocorticotropin and alpha-melanotropin. The DSIP immunoreactive cells in the adrenal medulla were identical with a major population of the noradrenaline-storing cells. High-performance liquid chromatography of tissue extracts revealed one major peak of DSIP-like immunoreactivity which did not coelute with synthetic DSIP. The immunoreactive material may represent N-terminally truncated fragments of DSIP. The present results suggest that the anterior and intermediate lobes of the pituitary and the adrenal medulla are potential sources of DSIP-like peptides.
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PMID:Immunoreactive delta sleep-inducing peptide in pituitary adrenocorticotropin/alpha-melanotropin cells and adrenal medullary cells of the pig. 303 39

Isolated tail arteries of rats were perfused and field-stimulated every 2 min with 2 pulses at 1 Hz. Different opioid peptides depressed the contractile responses to stimulation; their concentration-response curves showed a maximum at about 40% inhibition. The rank order of potency of the peptides was beta-endorphin (IC50 = 97 nmol/l) approximately equal to BAM-22P greater than FK-33824 greater than DAGO greater than [D-Ala2,D-Leu5]-enkephalin greater than or equal to metorphamide greater than dynorphin A-(1-13) approximately equal to [Met5]enkephalin. All these substances have in common a certain activity at opioid mu-receptors, although the enkephalins are preferential delta-, and the dynorphins preferential kappa-agonists. However, the selective delta-agonist [D-Pen2,L-Pen5]enkephalin was ineffective at up to 10 mumol/l, and the kappa-agonists ethylketocyclazocine and U-50488 acted only at concentrations higher than 3 mumol/l. Whereas the effects of beta-endorphin, DAGO and [D-Ala2,D-Leu5]enkephalin could be reduced by the mu-preferential antagonist naloxone, the effects of ethylketocyclazocine and U-50488 were not changed. The delta-selective antagonist ICI 174864 did not influence the action of [D-Ala2,D-Leu5]enkephalin. Naloxone in a concentration (1 mumol/l) which nearly abolished the effect of DAGO 3 mumol/l, slightly enhanced responses to stimulation. Neither beta-endorphin nor DAGO influenced vasoconstriction evoked by the application of noradrenaline or adenosine triphosphate; U-50488 reduced it. In arteries preincubated with [3H]noradrenaline DAGO depressed, whereas naloxone enhanced the tritium overflow and vasoconstriction evoked by field stimulation (0.4 Hz, 24 pulses every 14 min). In addition, naloxone antagonized the effect of DAGO.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Beta-endorphin-sensitive opioid receptors in the rat tail artery. 303 89

The tail pinch (t-p) method added to a basal restraint stress produced inhibition of the stress-induced hyperglycemia, an effect that was neutralized with intrathecal anesthesia but not with intracerebroventricular (i.c.v.) naloxone (50, 100, 1000 ng/100 g) or with intraperitoneal naloxone injections (0.1-0.3 mg/100 g). A similar negative result was obtained with i.c.v. administration of 500 and 1000 ng/100 g of beta-endorphin. In contrast, a single i.c.v. injection of 1000 ng/100 g of Met-enkephalin reproduced the t-p inhibitory effect. The latter was not elicited by i.c.v. FK 33824, an enkephalin analogue, a result that supports the specific participation of the delta-opioid receptors. The results obtained with central alpha-adrenoceptor antagonists and central noradrenergic chemical destruction, or central alpha-adrenoceptor agonists, support the production of a reinforcement of the alpha-adrenoceptor stress stimulation by the t-p procedure, probably through noradrenaline and enkephalin mediation.
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PMID:Inhibition of stress-induced hyperglycemia by tail pinching or intraventricular enkephalin administration in the rat. 304 94

An association between increased blood pressure levels and hypoalgesia has been reported in the experimental animal and in man. The relation between pain perception and cardiovascular function is however still obscure. In order to gain some insight into this aspect, normotensive subjects with low and high tolerance to pain, as assessed by tooth pulp stimulation, were compared for blood pressure and heart rate during cold pressor test, 24 hr urinary catecholamines, supine and upright PRA and plasma beta-endorphin levels. No significant difference was observed between the two groups for casual blood pressure, heart rate and PRA. Compared to subjects with low tolerance to pain, those with high tolerance to pain were significantly older and had: 1) significantly higher levels of diastolic blood pressure and of beta endorphin levels during cold pressor test; 2) significantly higher beta-endorphin levels after cold pressor test; 3) a significantly higher excretion of noradrenaline (but not of adrenaline and dopamine).
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PMID:Relationship between pain sensitivity, cardiovascular reactivity to cold pressor test and indexes of activity of the adrenergic and opioid system. 307 26

Mediobasal hypothalamus tissue (MBH) from adult male rats was incubated in Krebs-Ringer bicarbonate medium (KRB). KRB was changed at 15 min intervals and the concentration of immunoreactive beta-endorphin (beta-ENDi) in the medium was measured by radioimmunoassay. Incubation of MBH tissue in normal KRB resulted in a constant release rate of beta-ENDi of approximately 1% of the tissue content per h. KRB containing 45 mM K+ causes a two fold increase in the release rate of beta-ENDi which was Ca2+ dependent. Dopamine (0.01-1.0 microM) inhibits both the spontaneous and the K+-stimulated release of beta-ENDi in a dose related manner. The dopamine receptor blocking agent haloperidol prevents this inhibitory effect of dopamine. The selective D-1 receptor agonist SKF 38393 does not affect the release rate of beta-ENDi; whereas the selective D-2 receptor agonist LY 141865 inhibits both the spontaneous and K+-stimulated release of beta-ENDi. The effects of LY 141865 can be blocked by (-)-sulpiride, a selective D-2 receptor antagonist. Norepinephrine only weakly inhibits the K+-stimulated release of beta-ENDi, an effect that can be blocked by haloperidol but not by the alpha-adrenoceptor blocker phentolamine. At concentrations tested (0.01-1.0 microM), isoproterenol, 5-hydroxytryptamine, carbachol and 8-Br-cAMP (1.0 microM) do not affect beta-ENDi release. It is concluded that dopamine can inhibit the release of beta-ENDi from hypothalamic neurons via a D-2 receptor mechanism.
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PMID:Dopamine inhibits the release of immunoreactive beta-endorphin from rat hypothalamus in vitro. 315 84

Peripheral venous plasma free and sulfoconjugated catecholamines, dopamine (DA), noradrenaline (NA) and adrenaline (A) were measured in normal men (n = 6-7) during conditions significantly altering adrenal and sympathoadrenal function (influence of corticotropin, furosemide, hypoglycaemia and clonidine), after dopamine receptor blockade with metoclopramide and after meals. Median (range) basal plasma free DA concentration was 0.13 (0-0.72) nmol/l and median (range) basal plasma conjugated DA concentration was 15.16 (6.34-45.03) nmol/l. Meals increased plasma sulfoconjugated DA markedly from a median value of 14.97 nmol/l during fasting experiments to a median value of 33.01 nmol/l (p less than 0.05). Plasma free DA did not change in the meal experiments. No changes in plasma DA were observed after administration of corticotropin, furosemide, clonidine, and metoclopramide or during hypoglycaemia. The results suggest that plasma sulfoconjugated DA is derived at least in part from the gastrointestinal tract and not from the sympathoadrenomedullary system as hitherto proposed.
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PMID:Plasma free and sulfoconjugated dopamine in man: relationship to sympathetic activity, adrenal function and meals. 316 58

The sauna induces changes in the secretion of hormones, some similar to changes induced in any other stress situation and others characteristic of exposure to the sauna. Noradrenaline is usually the only catecholamine raised by the sauna in people accustomed to it. The secretion of the antidiuretic hormone is increased and the renin-angiotensin-aldosterone system is activated. The concentrations of the growth hormone and prolactin, in particular, secreted from the anterior pituitary are increased in the circulation. The concentration of the immunoreactive beta-endorphin in blood may also increase which may reflect the feeling of pleasure or, on the other hand, discomfort induced by the sauna. The views on the effects of the sauna on the secretion of the ACTH and cortisol are partly contradictory, probably due to differing ways of taking the sauna bath. In Finnish sauna takers the concentration of cortisol in blood is not usually increased. The changes induced by the sauna in various hormone concentrations in the circulation are, however, normalized within a couple of hours after the heat stress.
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PMID:How the sauna affects the endocrine system. 321 98

The neuroendocrine and cardiovascular responses to endotoxin administration and the effects of subsequent high-dose corticosteroid therapy have been investigated in dogs. Shock was induced in anaesthetised animals by a large bolus of E. coli endotoxin (5 mg/kg) followed by a continuous infusion (2 mg/kg per hour). One hour after induction of shock, the circulating volume was expanded using a colloidal gelatin solution. Fifteen minutes later, one group of five animals received a bolus of methylprednisolone sodium succinate 30 mg/kg, while a control group of five animals was given an equivalent volume of isotonic saline. The administration of endotoxin produced reductions in mean arterial pressure, cardiac index and left ventricular dp/dtmax, together with increases in systemic and pulmonary vascular resistances. These haemodynamic changes were associated with increases in arterial plasma levels of adrenaline, noradrenaline, cortisol, immunoreactive beta-endorphin and immunoreactive metenkephalin. Cardiovascular improvement followed volume replacement and was associated with reductions in circulating catecholamines. No significant haemodynamic or neuroendocrine changes were demonstrated in the 2 h following steroid therapy.
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PMID:Neuroendocrine and cardiovascular responses to high-dose corticosteroid therapy in canine endotoxin shock. 322 57


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