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 effect of the treatment with guanfacine on the activity of the adreno-sympathetic system, beta-thromboglobulin, beta-endorphin, and blood lipids was studied in 30 patients with the primary arterial blood hypertension. It was found that guanfacine significantly decreases plasma noradrenaline, adrenaline, and dopamine. Moreover, it decreases the excretion of noradrenaline, adrenaline and 4-hydroxy-3-methoxy-phenylglycol. These effects correlate with the drop in both systolic and diastolic blood pressure. A decrease in plasma renin activity was also observed. It correlated with the blood pressure drops. Guanfacine increased beta-endorphin levels while beta-thromboglobulin, total cholesterol and triglycerides levels remained unaffected. The authors suggest that the hypotensive effect of guanfacine is related to the decrease in adreno-sympathetic system activity and plasma renin activity and no effect on the erythrocyte activity and lipids metabolism.
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PMID:[Effect of long-term treatment with guanfacine on selected humoral metabolic indices in patients with primary hypertension]. 253 May 2

To assess changes of beta-endorphin during intense endurance exercise, ten nonspecifically trained volunteers (aged 25.7 +/- 2.9 years) were subjected to an exhaustive endurance test on a cycle ergometer at the work load of the individual anaerobic threshold (IAT) determined in a preparatory graded exercise test. Prior to, in 25-min intervals during, and repeatedly subsequent to exercise venous blood samples were drawn to measure the levels of beta-endorphin (beta-E), cortisol (C), adrenaline (A), and noradrenaline (NA). In addition, lactate, heart rate, and rate of perceived exertion were determined. The levels of beta-E remained unchanged during the first 50 min; between the 50th and 75th min beta-E increased by 82% (p less than 0.01). At the end of the exercise (mean exercise time: 89 min), a beta-E level three times the resting level was measured. The maximum exercise-induced increase of beta-E showed a positive correlation to endurance capacity (W.kg-1 of IAT): r = 0.74; p less than 0.05. C exhibited similar changes to beta-E, but the onset of increase was delayed if compared with beta-E; there was a close correlation between these two stress hormones (75th min of exercise: r = 0.91; p less than 0.001). The catecholamines A and NA increased linearly during exercise, without a correlation with the behavior of beta-E being established.
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PMID:Beta-endorphin, catecholamines, and cortisol during exhaustive endurance exercise. 253 79

During a 5 month, double blind crossover study of the clinical effect of cyclobenzaprine on 7 patients with fibrositis, weekly measurements were done of plasma beta-endorphin (endorphin, prostaglandin E (PGE) and catecholamines). Endorphin levels were normal but varied with tender point tenderness. Mean plasma dopamine and PGE were elevated. Norepinephrine was normal to very high while epinephrine levels were continuously low to normal. We conclude that patients with fibrositis have a neurotransmitter plasma profile like other chronic pain states having stress and increased vasomotor activity with the possible exception of having low circulating epinephrine. This disparity may mark a failure of central nervous system pain modulation in fibrositis.
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PMID:The plasma endorphin, prostaglandin and catecholamine profile of patients with fibrositis treated with cyclobenzaprine and placebo: a 5-month study. 253 82

The dog pituitary pars intermedia (PI) appears to consist of relative large numbers of ACTH-containing cells in addition to the more abundant alpha MSH-containing cells. Since regulation of PI secretion probably varies across mammalian species, this study was undertaken to identify substances potentially involved in the control of dog PI POMC peptide secretion and to determine if these substances altered the secretion of immunoreactive (IR) ACTH and IR-alpha MSH in a parallel fashion. Pituitary neurointermediate lobes from dogs were collected and dispersed, and the PI cells obtained were perifused. For comparison, rat PI and pars distalis (PD) cells as well as dog PD cells were similarly collected and perifused. Dog PI cells secreted IR-alpha MSH at a basal rate of 125 +/- 59 (mean +/- SD) pg/min.10(5) cells and IR-ACTH at a rate of 40 +/- 9 pg/min.10(5) cells (molar IR-alpha MSH/IR-ACTH = 10). In contrast, secretion rates for IR-alpha MSH and IR-ACTH from perifused rat PI cells were 171 +/- 108 and 3 +/- 2 pg/min.10(5) cells, respectively (molar IR-alpha MSH/IR-ACTH = 179). Using Sephadex G-50 gel filtration chromatography, virtually all of the IR-beta-endorphin secreted by dog PI cells eluted near beta-endorphin (1-31). In addition, all of the IR-alpha MSH secreted by dog PI cells coeluted with synthetic alpha MSH on the G-50 column, but IR-ACTH appeared in two peaks, one eluting near porcine ACTH-(1-39) and another, apparently larger mol wt species. Dopamine and somatostatin were found to inhibit the secretion of IR-alpha MSH and IR-ACTH from perifused dog PI cells in a parallel and dose-dependent fashion. Norepinephrine and epinephrine similarly inhibited POMC peptide secretion, but this effect was blocked by haloperidol, suggesting that it was mediated through a dopamine receptor. CRF stimulated the secretion of both hormones from dog PI, and this effect was abolished by treatment of the cells with either dopamine or somatostatin. Cortisol had no effect on either basal or CRF-stimulated secretion of IR-alpha MSH or IR-ACTH from dog PI cells, but it did inhibit CRF-stimulated IR-ACTH from perifused dog PD. These results suggest that 1) dog PI secretes considerably more IR-ACTH than that in the rat; 2) the probable separate cell sources of IR-alpha MSH and IR-ACTH in dog PI are regulated in an identical fashion; and 3) dopamine, somatostatin, and CRF may function in the physiological or pathophysiological regulation of dog PI.
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PMID:Regulation and secretion of proopiomelanocortin peptides from isolated perifused dog pituitary pars intermedia cells. 253 71

Neuropeptide Y (NPY) administration increases both hypothalamic corticotropin-releasing factor-like immunoreactivity (CRF-ir) and plasma adrenocorticotropin (ACTH). The dependence of these effects on noradrenaline and adrenaline was investigated by selectively depleting these neurotransmitters with 6-hydroxydopamine (6-OHDA) prior to administration of NPY. This combined treatment decreased hypothalamic CRF-ir (P less than 0.025), an effect isolated to the median eminence (P less than 0.025), whereas plasma ACTH increased greatly compared to 6-OHDA treatment alone (P less than 0.0005). In order to further investigate the potential mechanism of this NPY effect, the alpha 2-adrenergic agonist clonidine was administered to normal rats. This treatment increased plasma ACTH (P less than 0.005) and decreased hypothalamic CRF-ir (P less than 0.025), an effect localized to the median eminence (P less than 0.01). The results from both of these treatments are consistent with increased release of hypothalamic CRF. These data imply that the NPY-induced effects are dependent on normal noradrenergic/adrenergic neurotransmission. Depletion of these neurotransmitters allowed NPY to profoundly stimulate CRF release with no evidence for alteration in synthesis, a result common to alpha 2 stimulation.
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PMID:Neuropeptide Y-induced effects on hypothalamic corticotropin-releasing factor content and release are dependent on noradrenergic/adrenergic neurotransmission. 255 61

Recent evidence has suggested that stress may suppress the immune system and increase the frequency and severity of viral and neoplastic disease. The mechanisms for stress-induced modulation of immune function are unclear, but several neuropeptides are thought to be involved. Because macrophages play an important role in the host defense against infection and neoplasia, several stress-related neuropeptides were screened in efforts to determine whether these substances affect macrophage-mediated tumoricidal activity. Adrenocorticotropin and noradrenaline each completely blocked the capacity of mouse recombinant interferon-gamma (INF-gamma) to activate murine peritoneal macrophages to a tumoricidal state as measured by the lysis of 125I-UdR-labeled melanoma target cells. Vasoactive intestinal peptide significantly potentiated the suppressive effects of noradrenaline. In contrast, neurotensin markedly enhanced the cytolytic capability of peritoneal macrophages activated with INF-gamma. Several other neuropeptides, including substance P, alpha-endorphin, beta-endorphin, Leu-enkephalin, and Met-enkephalin, had no effect on macrophage activation. These findings demonstrate that selected stress-related neuropeptides and neurohormones significantly modulate the capacity of macrophages to attain a tumoricidal state and suggest that alteration of macrophage function by neuropeptides may be a prominent feature of stress-induced enhancement of neoplastic disease.
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PMID:Modulation of macrophage-mediated tumoricidal activity by neuropeptides and neurohormones. 258 37

Peripheral neuropathy is a correlate of experimental diabetes induced in rats by means of a single injection of alloxan. The autonomic and enteric innervation of the gut are profoundly affected in the small intestine of such animals. A complex process of denervation and hyperinnervation of the gut wall of diabetic animals is observed. It was previously reported that the cholinergic parasympathetic innervation of the intestine is markedly reduced. We have found that noradrenergic sympathetic axons hyperinnervate the duodenum of diabetic rats, whereas noradrenaline levels are significantly reduced in the jejunum. The putative enteric neurotransmitter dopamine is also present in higher levels in the duodenum. The intrinsic peptidergic neurons of the gut are deeply affected as well in diabetic rats. Substance P and met-enkephalin content are remarkably reduced throughout the small intestine, whereas vasoactive intestinal polypeptide levels (VIP) are significantly increased in the duodenum. Indeed, immunocytochemical staining of the ileum did reveal hypertrophy of VIP-positive axons in diabetic rats. The intrinsic serotoninergic innervation of the gut is apparently unaffected. Our results indicate that the changes of gut innervation observed in experimental diabetes are consistent with increased content and also likely with hyperinnervation by the neuronal systems involved in smooth muscle relaxation and decreased content and with denervation by those systems with smooth muscle contraction properties. Such a perturbed gut innervation may be responsible of the gastrointestinal dysfunctions that are among the most common complications of diabetes.
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PMID:Denervation and hyperinnervation in the nervous system of diabetic animals. I. The autonomic neuronal dystrophy of the gut. 259 79

Eight healthy young men were studied during three periods of heat exposure in a Finnish sauna bath: at 80 degrees C dry bulb (80 D) and 100 degrees C dry bulb (100 D) temperatures until subjective discomfort, and in 80 degrees C dry heat, becoming humid (80 DH) until subjective exhaustion. Oral temperature increased 1.1 degrees C at 80 D, 1.9 degrees C at 100 D and 3.2 degrees C at 80 DH. Heart rate increased about 60% at 80 D, 90% at 100 D and 130% at 80 DH. Plasma noradrenaline increased about 100% at 80 D, 160% at 100 D and 310% at 80 DH. Adrenaline did not change. Plasma prolactin increased 2-fold at 80 D, 7-fold at 100 D and 10-fold at 80 DH. Blood concentrations of the beta-endorphin immunoreactivity at 100 D, adrenocorticotropic hormone (ACTH) at 100 D and 80 DH, growth hormone at 100 D and testosterone at 80 DH also increased, but cortisol at 80 D and 100 D decreased. The plasma prostaglandin E2 and serum thromboxane B2 levels did not change. Patterns related to heat exposure were observed for heart rate, plasma noradrenaline, ACTH and prolactin in the three study periods.
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PMID:Haemodynamic and hormonal responses to heat exposure in a Finnish sauna bath. 275 81

The expression of opioid receptors and GTP-binding proteins was studied in 14 pheochromocytomas. The amounts of [3H]diprenorphine bound to membranes varied from 13 to 62 fmole/mg protein, but significantly higher in adrenaline-secreting tumors than in noradrenaline-secreting tumors. None of [3H]DADLE, [125I]beta-endorphin or [3H]ethylketocyclazocine binding was correlated with [3H]diprenorphine binding. Gpp(NH)p inhibition of [3H]DADLE binding was evident in all four normal human adrenal medullae but in only 8 out of 14 pheochromocytomas. The extent of Gpp(NH)p inhibition was not correlated with the amount of pertussis toxin (PT)-sensitive GTP-binding proteins as measured by PT-catalyzed [32P]ADP-ribosylation. The present findings suggest that opioid receptors and PT-sensitive GTP-binding proteins are variously expressed in transformed chromaffin cells, pheochromocytoma.
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PMID:Varying expression of opioid receptors and GTP-binding proteins in human pheochromocytomas. 282 58

A non-surgical, non-stressful technique was used for collection of pituitary venous blood from five conscious horses every minute for two 10-min periods before and during isolation from the herd, which caused a predictable, yet humane and physiological, emotional stress. Pituitary blood was also sampled every 5 min for two approximately 90-min periods before and after isolation, while jugular blood was sampled every 15 min throughout the experiment. During isolation, all horses became agitated, hyperventilating and sweating. Packed red cell volume increased, as did pituitary venous concentrations of adrenaline (mean +/- S.E.M. concentration before isolation, 621.5 +/- 112.3 pmol/l; peak during isolation, 2665.4 +/- 869.8 pmol/l; P less than 0.05) and noradrenaline (before, 871.8 +/- 111.8 pmol/l; peak, 2726.1 +/- 547.4 pmol/l; P less than 0.02). Concentrations of arginine vasopressin (AVP) were higher in pituitary venous but not in jugular blood during isolation than during the preceding 10-min period (P less than 0.05). Although AVP secretion increased in all horses, in three of the five it rose dramatically in the first minute of isolation to 25.7 (horse 1), 13.6 (horse 4) and 145.1 (horse 5) times the level in the last sample collected before isolation. Mean pituitary venous concentrations of ACTH and alpha-MSH increased during isolation in the three horses which had large increases in AVP secretion, but, overall, stress did not significantly affect ACTH or alpha-MSH secretion. Similarly, mean jugular cortisol levels were not significantly altered by isolation. However, the magnitudes of ACTH, AVP and alpha-MSH responses to isolation were negatively correlated with the jugular cortisol level before isolation. The changes in pituitary venous concentrations of ACTH and AVP were synchronous under resting conditions, whether samples were collected at intervals of 1 (P less than 0.01) or 5 (P less than 0.005) min; however, this synchrony was lost during isolation. The changes in pituitary venous concentrations of ACTH and alpha-MSH were synchronous both at rest (P less than 0.025 for 1-min sampling, P less than 0.01 for 5-min sampling) and during isolation (P less than 0.01). We conclude that isolation stress increases AVP secretion and may alter the temporal relationship between pituitary venous concentrations of AVP and ACTH. Furthermore, the magnitude of the responses of AVP, ACTH and alpha-MSH to isolation is significantly affected by the prevailing cortisol level.
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PMID:Effect of isolation stress on concentrations of arginine vasopressin, alpha-melanocyte-stimulating hormone and ACTH in the pituitary venous effluent of the normal horse. 283 3


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