Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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 present study was conducted to characterize the in vivo effects of epinephrine administration on levels of pituitary cyclic AMP and plasma hormones. Rats were injected with saline or epinephrine bitartrate (1 mg/kg lP) and sacrificed by decapitation 1, 5, 15, 30 or 60 min post-injection. Levels of pituitary cyclic AMP and plasma ACTH, beta-endorphin, beta-LPH, corticosterone and prolactin were determined by radioimmunoassays. The injection procedure itself was somewhat stressful as demonstrated by increased levels of plasma prolactin and ACTH 5 min following either saline or epinephrine injection. This "stress" response was rapid and short-lasting for the pituitary hormones. The response of the adrenal hormone, corticosterone, to saline injection was slower in onset and longer in duration. Pituitary cyclic AMP levels did not increase following saline injection. Epinephrine-injected animals displayed markedly elevated plasma levels of ACTH, beta-endorphin and beta-LPH at 15, 30 and 60 min as compared to control or saline-injected rats. In addition, levels of pituitary cyclic AMP were increased over 10 fold at these times. Levels of plasma prolactin, a stress-responsive hormone, were not significantly increased in epinephrine-injected animals as compared to saline-injected rats indicating that these later responses seem to be specific to epinephrine rather than to stress.
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PMID:Pituitary cyclic AMP and plasma hormone responses to epinephrine administration in vivo. 302 35

The potential involvement of the sympathoadrenal system in stress-induced secretion of peptides from the intermediate lobe of the pituitary gland and the activation of the pituitary-adrenal axis was studied. Male Wistar rats were subjected to control procedures, to sympathectomy by chronic administration (8 weeks) of guanethidine and/or to medullectomy by adrenal enucleation 9 weeks prior to exposure to forced immobilization stress for various periods of time. In intact or sham-operated rats, immobilization caused a prompt increase of circulating norepinephrine, epinephrine (EPI), corticosterone and of immunoreactive adrenocorticotropic hormone (ACTHi), alpha-melanocyte-stimulating hormone (alpha-MSHi) and beta-endorphin (beta-ENDi). Peak levels of pituitary hormones were found after 10 min of stress exposure, but fell to less than 30% of these levels after 2.5 h of immobilization. Adrenal medullectomy, which abolished the stress-induced release of EPI, reduced the acute increase of plasma alpha-MSHi and beta-ENDi, but did not influence the acute increase of plasma ACTHi during immobilization stress. Also in medullectomized plus sympathectomized rats, the initial stress response of circulating ACTHi was not different from that of controls. Adrenal medullectomy with or without additional sympathectomy caused a marked increase in plasma ACTHi concentrations after prolonged stress exposure. We conclude that: catecholamines originating from the adrenalmedulla facilitate the stress-induced secretion of intermediate lobe peptides (alpha-MSHi, beta-ENDi); catecholamines from the sympathoadrenomedullary system do not contribute to the acute release of ACTH during immobilization stress; the sympathoadrenomedullary system is involved in the secondary reduction of circulating ACTHi levels seen during prolonged stress.
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PMID:Sympathoadrenal activity facilitates beta-endorphin and alpha-MSH secretion but does not potentiate ACTH secretion during immobilization stress. 303 40

The possible involvement of endogenous opioid peptides in the development of the facilitatory effect of adrenaline on memory has been investigated. For this purpose post-training administration of adrenaline and/or naloxone was carried out in rats tested in an inhibitory avoidance paradigm and subjected or not to pre-training (extensive familiarization with the training situation prior to the acquisition trial). Adrenaline injected subcutaneously in a dose of 500 micrograms/kg facilitated retention performance in rats both subjected or not to pre-training. Naloxone administered SC (400 micrograms/rat) did not influence retention behaviour in rats subjected or not to pre-training, nor did ICV (0.80 ng/rat) administration. Interestingly, the opiate antagonist when injected SC (400 micrograms/rat) prevented the facilitatory effect exerted by adrenaline in pretrained as well as in not pre-trained rats. However, ICV administration of naloxone (0.80 microgram/rat) dit not influence the behavioral effects exerted by the bioamine. These data suggested a role of endogenous opioid peptides on the facilitatory effect of adrenaline on memory, possibly independent of novelty factors and thus of the brain beta-endorphin system. In addition, our results point to the periphery as the most likely site for such interaction.
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PMID:Naloxone prevents the facilitatory effect upon retention induced by adrenaline administration in rats. 312 49

We examined the effects of intraventricular (Ivt) administration of beta-endorphin (beta E) on preovulatory LH release, ovulation, and the mechanism that may be involved in opioid action. Female rats were implanted with permanent cannulae in the third ventricle of the brain and were allowed to recover 4-day estrous cyclicity. Intrajugular cannulae were placed on the morning of proestrus. Thereafter, they received Ivt either saline (2 microliter) or beta E (10 micrograms/2 microliter) at 1300, 1430, and 1600 h. In addition, at 1600, 1700, and 1800 h, they were injected Ivt with either vehicle (cerebrospinal fluid or saline) or one of the following compounds: epinephrine (15.3 micrograms), norepinephrine (15.3 micrograms), or prostaglandin E2 (6 micrograms). Blood samples for LH measurements were taken 0, 10, 30, and 60 min after the additional injections at 1600 and 1700 h. beta E blocked the preovulatory LH surge and ovulation. Administration of the opiate receptor antagonist naloxone (2 mg/kg) reversed these effects. Epinephrine stimulated a small discharge of LH only after a second E injection in the beta E-treated rats, but this was insufficient to restore ovulation. On the other hand, prostaglandin E2 reversed the beta E blockade of the LH surge and ovulation. These studies suggest that beta E blocks ovulation and the LH surge primarily by suppressing either the influx or adrenergic expression of the spontaneous neurogenic stimuli responsible for the preovulatory LH discharge and not by evoking a general decrease in the secretory response of the LHRH neurons.
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PMID:Reversal of beta-endorphin-induced blockade of ovulation and luteinizing hormone surge with prostaglandin E2. 316 May 73

Macrophages have been shown to possess cell surface receptors for opiates and catecholamines. The abilities of these ligands to affect RAW264 macrophage antibody-dependent effector activity directed against sheep red blood cells were tested. Phagocytosis was measured by the uptake of 51Cr labeled erythrocytes and optical microscopy. Cytolysis was measured by 51Cr-release assays. Met-enkephalin increased specific antibody-dependent phagocytosis in a dose-dependent fashion; the optimal dose was found to be 10(-8) M. Epinephrine diminished phagocytosis in a dose-dependent manner exhibiting a maximal inhibition at 10(-4)-10(-5) M. This inhibition can be blocked by propranolol. The combined effects of simultaneous treatment with met-enkephalin and epinephrine were measured. At the several doses tested, the combined effects of these two ligands on the amount of phagocytosis were equivalent to or more inhibitory than epinephrine alone. Thioglycolate-elicited murine peritoneal macrophages demonstrated similar responses to epinephrine, met-enkephalin, and their combination. Therefore, in vitro models more closely approximating in vivo neuroregulation of macrophage function demonstrate phagocytic inhibition.
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PMID:Combinative ligand-receptor interactions: epinephrine depresses RAW264 macrophage antibody-dependent phagocytosis in the absence and presence of met-enkephalin. 334 39

Gonadal, adrenal, and thyroid functions were evaluated in 70 men seropositive for human immunodeficiency virus (HIV) infection, clinically categorized as asymptomatic (n = 19), AIDS-related complex (ARC) (n = 9), or acquired immunodeficiency syndrome (AIDS) (n = 42). Twenty of 40 men (50 percent) with AIDS were hypogonadal. Mean serum testosterone concentrations in both ARC (292 +/- 70 ng/dl) and AIDS (401 +/- 30 ng/dl) men were significantly less than in asymptomatic (567 +/- 49 ng/dl) or normal men (608 +/- 121 ng/dl). Of these hypogonadal men, 18 of 24 (75 percent) had hypogonadotropic hypogonadism. Seven of eight hypogonadal men (88 percent) had a normal gonadotropin response to gonadotropin-releasing hormone administration. Hypogonadism correlated with lymphocyte depletion and weight loss. Adrenal cortisol reserve, evaluated by adrenocorticotropin stimulation, was normal in 36 of 39 patients (92 percent) with AIDS. Indices of thyroid function were normal with the exception of one ARC man with a low free thyroxine index. In conclusion, hypogonadism is common in men with HIV infection and may be the first or most sensitive endocrine abnormality.
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PMID:Endocrine disorders in men infected with human immunodeficiency virus. 334 69

Adrenal enkephalin and enkephalin-containing peptides were studied during postnatal development in normotensive (WKY) and spontaneously hypertensive rats (SHR). The effect of chronic treatment with the ganglionic blocker chlorisondamine (5 mg/kg) was also assessed. Free enkephalin immunoreactivity and total enkephalin immunoreactivity, as determined by enzymatic digestion of large enkephalin containing fragments, were quantitated in the adrenal glands at 11 days and 7, 16, and 24 weeks of age. Both total and free metenkephalin were significantly diminished in the adrenal of SHR when compared to WKY at all ages tested. The analysis of the chromatographic profile showed that SHR displayed reduced levels of high and low molecular weight materials at 11 days and 16 weeks of age; however intermediate compounds were high in the glands of these animals. Similar increased values for free met-enkephalin were found in adrenals of WKY and SHR after ganglionic blocker treatment, which means that the relative increase was larger in SHR than WKY; while for total enkephalin the relative increase and the concentration reached in SHR was about half of those presented in WKY. These and other results presented suggest that the basic alteration of the adrenal proenkephalin system of SHR may be due to a genetic reduction of proenkephalin levels. Otherwise, the free enkephalin decrease could be related to changes in nervous input to the adrenal gland.
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PMID:Adrenal proenkephalin-derived peptides during postnatal development in spontaneously hypertensive rats. 339 8

Hypotensive functional haemorrhage induced by venous pooling of blood in the legs has been reported to be characterized by a vasovagal reaction. In the present study these observations were extended by determination of the hormonal profile developed during progressive central hypovolaemia and an emotionally induced vasovagal syncope. In six subjects venous pooling resulted in normotensive central hypovolaemia, in one subject hypotensive central hypovolaemia was induced, and one subject experienced an emotionally induced vasovagal syncope. During normotensive central hypovolaemia heart rate increased from 58 +/- 4 to 76 +/- 4 beats min-1 (P less than 0.05) and cardiac output fell from 6.1 +/- 0.4 to 4.1 +/- 0.2 1 min-1. Pulse pressure and central venous pressure decreased from 64 +/- 4 to 53 +/- 4 mmHg, and from 8 +/- 2 to 3 +/- 2 mmHg, respectively. Adrenaline and noradrenaline increased from 87 +/- 10 to 120 +/- 20 pg/ml and from 196 +/- 33 to 370 +/- 50 pg/ml, respectively. Angiotensin II increased from 13 +/- 4 to 36 +/- 6 pg/ml and aldosterone from 63 +/- 9 to 180 +/- 27 pg/ml. In hypotensive central hypovolaemia the decrease in mean arterial pressure was accompanied by a decrease in heart rate and increments in the plasma concentrations of pancreatic polypeptide, indicating increased vagal activity and beta-endorphin, while plasma noradrenaline was unchanged. In emotionally induced syncope heart rate decreased to cardiac arrest for 13 s, associated with increments in the plasma concentrations of pancreatic polypeptide and beta-endorphin. It is concluded that normotensive functional haemorrhage in man is associated with increased sympathetic activity and that the qualitatively similar observations obtained during an emotionally and a hypovolaemic-induced hypotensive episode indicate that the hypotensive functional haemorrhage is characterized by a vasovagal reaction.
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PMID:Progressive central hypovolaemia in man--resulting in a vasovagal syncope? Haemodynamic and endocrine variables during venous tourniquets of the thighs. 360 88

The possible inotropic effects of all three classes of endogenous opioids were tested alone or in combination with noradrenaline, adrenaline, or carbachol on electrically stimulated atria isolated from male Sprague-Dawley rats. Noradrenaline (6.0 and 12 microM) and adrenaline (4.0 and 8.0 microM) injections caused marked but transient (5 min) dose-related increases in atrial tension compared with preinjection control values, whereas carbachol (0.14 and 1.4 microM) caused a more potent and prolonged (over 15 min) dose-related decrease in atrial tension development. Adrenal enkephalins (0.3-4.0 microM) of methionine enkephalin, leucine enkephalin, Met-enkephalin-Arg6-Phe7, and Met-enkephalin-Arg6-Gly7-Leu8, beta-endorphin (0.2-2.0 microM), or dynorphin A(1-13) (0.2-2.0 microM) did not change atrial tension for a 15-min postadministration test period. In addition, these opioids did not affect the positive inotropic effects of noradrenaline (12 microM) or adrenaline (8.0 microM) or the negative inotropic actions of carbachol (1.4 microM) when the same doses of noradrenaline, adrenaline, or carbachol were given alone. These data indicate that endogenous opioids given in micromolar concentrations tested did not affect atrial tension development of electrically stimulated rat atria. Comparing these data with those of past literature, it is suggested that circulating endogenous opioids probably do not have any direct effects on the rat myocardium to affect myocardial contractility.
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PMID:The effects of endogenous opioids on tension development of isolated, electrically stimulated rat atria. 362 Oct 71

A "closed space" subarachnoid hemorrhage (SAH) was produced experimentally in cats by rupture of the right middle cerebral artery to test the working hypothesis that a stressful event which provokes powerful sympathoadrenal discharge: causes a massive release of co-stored endogenous enkephalins together with catecholamines, induces an increased rate of opioid peptide precursor processing and/or synthesis, and eventually results in markedly elevated tissue levels of enkephalins relative to controls and to co-stored catecholamines. Adrenal medulla and other tissues were analyzed for met- and leu-enkephalins by RIAs and norepinephrine and epinephrine by HPLC-EC at 4 hrs, 3, 10, 16 and 30 days post-SAH. Catecholamines of adrenal medulla were already decreased at 4 hrs and by 3 days post-SAH depletion of epinephrine reached 86% and norepinephrine 53% compared to controls. Concurrently, at 4 hrs and 3 days post-SAH, the adrenal medulla was depleted 47% of met- and 53% of leu-enkephalins. By 10 days post-SAH, when catecholamines had regained control levels, met-enkephalin was elevated to 240% of control and 435% compared to the 3 day depletion; it remained elevated through 30 days post-SAH. In comparison, after 10 days reserpine treatment when catecholamines were markedly depleted, met-enkephalin rose to 970% and leu-enkephalin to 360% relative to controls, confirming recent reports in the literature. The data suggest that release of enkephalins originates primarily from epinephrine-type cells of the adrenal medulla in cat.
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PMID:Adrenal enkephalin and catecholamine contents following subarachnoid hemorrhage in cats. 376 79


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