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)

Electroconvulsive therapy is accompanied by an activation of the hypothalamic-pituitary-adrenal axis, resulting in a release of beta-endorphin from the anterior pituitary corticotrophs of humans. As a group, patients in our study demonstrated similar plasma beta-endorphin immunoreactivity response to their initial and final treatments. However, approximately half of the patients demonstrated greater beta-endorphin immunoreactivity release with their first seizure compared with their last seizure, and half of the patients demonstrated the opposite pattern. This difference was not explained by age, sex, unilateral vs bilateral treatments, sine wave vs brief pulse, or psychotropic or anticholinergic medication. Patients with constant seizure duration during the first and final treatments demonstrated a greater release of beta-endorphin immunoreactivity with the final treatment compared with the first treatment. Individuals with decreasing seizure duration during the course of the electroconvulsive therapy demonstrated a decreased beta-endorphin immunoreactivity response during their final treatment.
Arch Gen Psychiatry 1991 Jun
PMID:Heterogeneity in the beta-endorphin immunoreactivity response to electroconvulsive therapy. 203 37

1. The relationship between salmon calcitonin (S-CT) and opioid system was studied in isolated guinea-pig ileum. 2. Addition of S-CT (0.1 to 1.6 U/ml) to the organ bath did not modify the amplitude of the contractile response induces by electrical stimulation. 3. However, when tissues were incubated 30 min with S-CT (0.1 U/ml), the inhibitory effect of the release of endogenous opioids, met-enkephalin (1 microM) and morphine (0.2 microM) was significantly increased. 4. Our results suggest that some of the analgesic effects of S-CT could be attributed to an up-regulation of the opioid receptors.
Gen Pharmacol 1991
PMID:Calcitonin increases the inhibitory effect of opioids in guinea-pig ileum. 205 Feb 89

1. Modifications by stress of the effects of morphine on pituitary-adrenocortical activity were examined in the guinea-pig at different lengths of time. 2. An increase in plasma cortisol but not in beta-endorphin levels was obtained in guinea-pigs stressed for 60 min. 3. Morphine (50 mg kg i.p.) enhanced beta-endorphin and cortisol levels 5 min after injection and decreased beta-endorphin concentration 30 and 90 min after its administration. 4. In stressed guinea-pigs plasma beta-endorphin levels were reduced 5 min after morphine injection. 5. These results indicate that stress can alter the effects of morphine on pituitary-adrenal activity in the guinea-pig and that the type of modification may be dependent on the time of the sampling.
Gen Pharmacol 1991
PMID:Influence of stress in the effects of morphine on pituitary-adrenocortical activity in the guinea-pig. 205 15

Previous studies have shown that the release of melanotropin from frog neurointermediate lobes is under the control of two neuropeptides: thyrotropin-releasing hormone (TRH) stimulates, while neuropeptide Y (NPY) inhibits alpha-melanocyte-stimulating hormone (alpha-MSH) secretion from intact neurointermediate lobes in vitro. The aim of the present study was to investigate possible interactions between the two regulatory peptides at the pituitary level. Whole neurointermediate lobes or acutely dispersed pars intermedia cells from Rana ridibunda were perifused in vitro for 2 to 7.5 hr and the concentrations of alpha-MSH released into the effluent perifusate were monitored by radioimmunoassay. Administration of TRH (10(-7) M) or NPY (10(-7) M) to dispersed cells induced, respectively, marked stimulation or inhibition of alpha-MSH release. The effects of the two neuropeptides were similar to those observed using intact neurointermediate lobes, suggesting that TRH and NPY act directly on melanotropic cells. Perifused whole neurointermediate lobes were exposed to NPY (10(-8) to 3 x 10(-7) M) for 120 min and a single dose of TRH (10(-8) M) was administered during the prolonged infusion of NPY. Using this procedure, we observed a dose-dependent inhibition of TRH-evoked alpha-MSH release. These data support the concept that TRH and NPY act through a common intracellular pathway to regulate alpha-MSH release.
Gen Comp Endocrinol 1990 Jan
PMID:Neuropeptide Y inhibits thyrotropin-releasing hormone-induced stimulation of melanotropin release from the intermediate lobe of the frog pituitary. 210 15

Studies in depression using a maximal stimulatory dose of corticotropin releasing factor have concluded that elevated resting cortisol levels in depressed patients exert a negative feedback effect on the corticotroph, resulting in a decreased corticotropin response. In this preliminary report, we examine the effects of a submaximal dose of corticotropin releasing factor on the release of another corticotroph secretory product, beta-lipotropin-beta-endorphin. We observed a decreased beta-lipotropin-beta-endorphin response in depressed subjects, but a normal adrenal cortisol response. Although the total beta-lipotropin-beta-endorphin response was decreased, the initial secretory response did not differ between patients and normal controls. Rather, the patients appeared to turn off secretion faster. This rapid shutoff was seen in all patients regardless of resting cortisol levels, suggesting that resting cortisol levels alone do not explain the decreased response seen in depressed patients.
Arch Gen Psychiatry 1990 May
PMID:Beta-lipotropin-beta-endorphin response to low-dose ovine corticotropin releasing factor in endogenous depression. Preliminary studies. 213 63

We assessed the plasma corticotropin (adrenocorticotropic hormone) and cortisol responses to ovine corticotropin releasing hormone (oCRH) and the cerebrospinal fluid levels of CRH and corticotropin in alcoholics at various durations of abstinence and compared these variables with age-equivalent controls. Alcoholics who were tested at 1 week of abstinence (n = 11) demonstrated a significantly attenuated corticotropin response to oCRH compared with their response at 3 weeks of abstinence. Nine of these alcoholic patients demonstrated a significantly blunted corticotropin response at both 1 and 3 weeks of abstinence compared with controls (n = 15). A markedly exaggerated corticotropin response to oCRH, associated with tachycardia, was exhibited by 2 alcoholics at both 1 and 3 weeks of abstinence. Alcoholics who were abstinent greater than 3 weeks did not differ in their response to oCRH compared with controls. Controls demonstrated a significant inverse correlation between baseline cortisol levels and the cortisol response to oCRH. This correlation was not evident in any of the alcoholic groups, including those patients who were abstinent greater than 6 months. There was a positive correlation between cerebrospinal fluid concentrations of CRH and corticotropin in all patient groups. These findings indicated that alcoholics have significantly altered hypothalamic-pituitary-adrenal axis functioning up to 3 weeks following the cessation of drinking, with a more subtle impairment present for greater than 6 months following abstinence.
Arch Gen Psychiatry 1990 Apr
PMID:Hypothalamic-pituitary-adrenal axis functioning and cerebrospinal fluid corticotropin releasing hormone and corticotropin levels in alcoholics after recent and long-term abstinence. 215 79

In teleost fishes, the melanotropes of the neurointermediate lobe of the pituitary gland release numerous peptides--adrenocorticotropin (ACTH), melanotropin (MSH), lipotropin (LPH), corticotropin-like intermediate lobe peptide (CLIP), and endorphin--which are derived from the precursor molecule proopiomelanocortin. Superfused, isolated, dispersed goldfish neurointermediate lobe cell columns were used to investigate the release of immunoreactive (ir) alpha-MSH and ir ACTH from goldfish melanotropes. Stimulation of neurointermediate lobe cell columns with pulses of the structurally homologous peptides, Catostomus urotensin I (UI), ovine corticotropin-releasing factor (oCRF), or sauvagine, produced a significant increase in the concomitant release of ir alpha-MSH and ir ACTH. UI was two to three times as potent as ovine CRF or sauvagine. These studies suggest that CRF- and UI-like peptides stimulate the secretory activity of teleost melanotropes.
Gen Comp Endocrinol 1990 Jun
PMID:CRF, urotensin I, and sauvagine stimulate the release of POMC-derived peptides from goldfish neurointermediate lobe cells. 216 77

This immunocytochemical study of the pituitaries of the primitive actinopterygians, Acipenser transmontanus, Lepisosteus spatula, and Amia calva, showed a strict delineation between the hormonal fragments of proopiomelanocorticotropin (POMC) produced by corticotropes of the pars distalis and the melanotropes of the pars intermedia. Corticotropes were immunoreactive only for ACTH and not to either of the further degradation products, alpha-MSH or beta-endorphin. Melanotropes were shown to be immunoreactive to all three antisera but it is argued that immunoreactivity of melanotropes to ACTH antiserum is due to that antiserum's cross-reactivity with the cleavage product corticotropin-like intermediate peptide. The PAS positivity of both the corticotropes and the melanotropes of all three primitive fish argues for an ancient origin of a carbohydrate component of POMC and for its loss or reduction in teleosts where these cells are PAS negative.
Gen Comp Endocrinol 1990 Jun
PMID:Immunocytochemical location of pituitary cells containing ACTH, alpha-MSH, and beta-endorphin in Acipenser transmontanus, Lepisosteus spatula, and Amia calva. 216 79

1. In addition to their antihypertensive effect, ACE inhibitors have been reported to increase general well-being, general health and vitality and work performance. The cause of these effects is not known. A possible mechanism may be release of beta-endorphins. 2. In the present study changes in plasma concentration of beta-endorphins on days with ACE inhibitor treatment (n = 12) and on non-treatment control days (n = 12) were compared in 6 patients. 3. Both on control and treatment days the beta-endorphin level fell, by 7.1 and 10.0%, respectively, from 8.00 a.m. to 8.00 p.m., reflecting the known diurnal rhythm of this opioid. This difference between the control and treatment days is not statistically significant. 4. The study should be extended to determine endorphin concentration in the cerebrospinal fluid, and other opioids should be looked for.
Gen Pharmacol 1990
PMID:Effects of an angiotensin converting enzyme (ACE) inhibitor on plasma endorphin level. 217 36

Antisera raised against chum salmon prolactin (PRL), rainbow trout growth hormone (GH), mammalian adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone (TSH), and luteinizing hormone (LH) were used to study the chronological appearance of immunoreactivity for PRL, GH, ACTH, TSH, LH, and melanocyte-stimulating hormone (MSH) in the pituitary of sea bass larvae (Dicentrarchus labrax) during the first 26 days after hatching. The anti-ACTH gives positive immunostaining in the ACTH cells as well as in the MSH cells; however, the two cell types can easily be distinguished by their different localization in the pituitary: ACTH in the rostral pars distalis, MSH in the pars intermedia. The first day after hatching cells immunoreactive for TSH, GH and ACTH could already be noticed, ACTH reacted strong in the pars intermedia but very weak in the rostral pars distalis. Cells immunopositive for PRL became visible between Days 9 and 15. With anti-LH, no positive reaction could be obtained during the first 26 days after hatching.
Gen Comp Endocrinol 1990 Mar
PMID:Chronological appearance of the different hypophysial hormones in the pituitary of sea bass larvae (Dicentrarchus labrax) during their early development: an immunocytochemical demonstration. 218 61


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