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)

(1) The availability of short amino acid sequences of the naturally occurring ACTH 1-39 molecule has made it possible to separate the corticotropic characteristics of the parent molecule from its neurotrophic effects. Potent neurotrophic fragments are ACTH 4-10, an analog of ACTH 4-9 (Org 2766), and alpha-MSH (ACTH 1-13), peptide fragments that do not evoke corticosteroid secretion, yet clearly affect both the development and regeneration of peripheral nerve. (2) Early postnatal administration of either ACTH 4-10 or Org 2766 accelerates the neuromuscular development of the immature rat, increasing the contractile strength of the EDL muscle and inducing more rapid muscle contractions. Grasping strength and motor activity are increased; these are all changes indicative of more rapid neuromuscular maturation. Prenatal peptide treatment elicits a more complex pattern of response since administration early in gestation (GD 3-12) accelerates neuromuscular development whereas later administration (GD 13-21) decelerates maturation. (3) ACTH peptides have a similar accelerating effect on the morphology of the developing neuromuscular junction. At two weeks of age, nerve arborization is conspicuously increased by postnatal administration of either ACTH 4-10 or Org 2766, as is nerve terminal branching within the endplate itself. However, this is preceded by an initial depression of nerve branching in the 7-day-old rat pup. We conclude that while the developing neuromuscular system is sensitive to ACTH peptides, this susceptibility is age-related. The crucial role of these peptides may be limited to very brief, defined periods during which the peptides may interact with trophic or growth-associated substances, each of which may have its own decisive, circumscribed time frame of influence. (4) Perinatal administration of ACTH peptides affects CNS development. One measurable indication of this is an acceleration of eye opening. Early exposure to ACTH peptides has long-lasting effects on behavior, apparent when these animals are tested as adults. Increased spontaneous motor activity, heightened states of arousal and agitation, and changes in social behavior have been reported. Certain avoidance responses and tests of visual discrimination in male rats are improved by neonatal treatment with alpha-MSH. Overall motor activity is increased and the normal period of hyperactivity is initiated earlier. Male sexual behavior is decreased and sexually dimorphic behaviors in males are eliminated. alpha-MSH may alter the development of its own dopaminergic feedback circuitry while ACTH affects serotonin levels in the preoptic nucleus.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:ACTH modulation of nerve development and regeneration. 254 30

Fifteen white patients participated in this study of a family-practice-based smoking cessation program in which corticotropin (ACTH) was used to assist patients during the first one to two weeks of abstinence from nicotine. All patients were habitual smokers who had made one or more attempts to quit smoking before entering this program. Treatment consisted of three single intramuscular injections of ACTH. In most cases, declining doses of 160, 80, and 40 U were administered at three-day intervals. The decision to provide additional treatment was based on the response by each volunteer and the investigator's judgment. The mean duration of follow-up was 33 days (range, 17 to 49 days), with the exception of two patients, who have just recently completed therapy. Evidence supporting complete smoking cessation or a significant reduction (80% to greater than 90%) in the number of cigarettes smoked per day was achieved in 13 of the 15 patients. The single nonresponder expressed an initial interest in the program, but showed a lack of motivation thereafter. There was insufficient follow-up on one other patient, who has not been available for monitoring since completion of therapy. Symptoms associated with the tobacco withdrawal syndrome that were reported by the patients included mild irritability and restlessness.
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PMID:Repository corticotropin injection as an adjunct to smoking cessation during the initial nicotine withdrawal period: results from a family practice clinic. 255 99

We report here three patients with hypopituitarism accompanied by primary empty sella, whose first manifestations were various mental symptoms. Endocrine studies revealed that two patients showed panhypopituitarism and the other had isolated adrenocorticotropin (ACTH) deficiency. Although several different types of pituitary dysfunctions have been described in a mild form, empty sella is usually asymptomatic. Their first manifestations were mental symptoms; consciousness disturbance, psychomotor agitation, visual hallucination and delusion. Isolated ACTH deficiency is an uncommon disease which etiology is still undetermined. A case with isolated ACTH deficiency associated with an empty sella has been reported before. It is suggested that empty sella might have a role in pathogenesis of isolated ACTH deficiency. The empty sella was confirmed by metrizamide cisternography and magnetic resonance imaging (MRI). These imaging studies are good tools to disclose empty sella. Replacement with cortisone and levothyroxine resulted in an improvement in the mental symptoms in two patients with panhypopituitarism. No alteration was observed following cortisone administration in the patient with isolated ACTH deficiency. Delusion and visual hallucination in this patient poorly responded to treatment with neuroleptics.
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PMID:[Three patients with hypopituitarism accompanied by primary empty sella presenting mental symptoms]. 259 26

alpha-MSH-related compounds may prove to be clinically useful antipyretics since the parent peptide is extremely potent in reducing fever, it is effective when given orally, and it neither stimulates corticosteroid activity nor has marked melanotropic effects in man. To determine whether or in what doses alpha-MSH might cause harmful side-effects, we injected doses greatly exceeding those required to reduce fever into a lateral cerebral ventricle of afebrile rabbits. One hundred to seven hundred and fifty micrograms alpha-MSH caused large and prolonged reductions in body temperature and the dose-response relation was bell-shaped for both magnitude and duration. These doses caused no apparent injury to the animals. One mg alpha-MSH elicited hyperthermic responses that were variable in magnitude and duration. Animals that had previously received large doses of alpha-MSH (greater than or equal to 100 micrograms) did not develop hyperthermia, even when given 2 mg, indicating an acquired tolerance to this hyperthermic action of alpha-MSH. All animals, tolerant or previously uninjected, showed symptoms with doses greater than or equal to 1 mg alpha-MSH that included: increased salivation, agitation, ataxia, respiratory distress, and death (in 30% of the animals); those that recovered from these large doses resumed outwardly healthy appearance and behavior. Although alpha-MSH is toxic when given centrally in large doses, the 5000-fold difference between antipyretic and toxic doses indicates a wide safety margin should this peptide be used clinically as an antipyretic drug.
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PMID:Effects of massive doses of alpha-MSH on thermoregulation in the rabbit. 387 78

Tissue from histologically confirmed ACTH cell adenomas in Cushing's disease (CD) and Nelson's syndrome (NS) was gained by transsphenoidal surgery. Combined enzymatic and mechanic agitation of tumor tissue yielded a cell suspension. Aliquots of the cell suspension were transferred to superfusion chambers immediately after isolation and investigated for ACTH and beta-endorphin production. Feedback action of cortisol (CO) and dexamethasone on basal hormone production and on lysine vasopressin (LVP) induced ACTH secretion were studied. Adenomatous tissue and anterior lobe tissue from the same patient in CD could be investigated simultaneously in 4 cases. The paraadenomatous tissue showed depression of basal and LVP-induced ACTH secretion. In all adenomatous tissues investigated there was missing or reduced suppression of basal ACTH secretion by physiological levels of CO. CO not only failed to suppress LVP-induced ACTH secretion but also seemed to enhance LVP stimulation in some experiments. This study confirms former results, that a missing or inversed feedback action or glucocorticoids in adenoma cells is a mechanism involved in the pathological ACTH secretion in CD and NS. Bioassayable and immunoreactive ACTH from media of superfusion and short-term static incubation were compared with beta-endorphin and beta-LPH in an assay detecting these two peptides with equimolar sensitivity. Secretory patterns were basically parallel but great differences showed in quantities of hormones secreted. In addition, Sephadex G-50 gel chromatography was performed to separate beta-endorphin from beta-LPH and to calculate the ratios. These profiles show great variations between different adenomas.
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PMID:In vitro secretion of ACTH, beta-endorphin and beta-lipotropin in Cushing's disease and Nelson's syndrome. 626 13

The endogenous opiate-like peptides, beta-endorphin, methionine- and leucine-enkephalin have been investigated in unanaesthetized cats after intracerebroventricular injection. beta-Endorphin produced marked and prolonged psychomotor stimulation (restlessness, apprehension, looking around, vacant stare and impelling locomotion), accompanied by pupillary dilation and tremor which was prevented by nalorphine. In contrast to beta-endorphin, the enkephalins did not cause affective behavioural phenomena. However, the enkephalins evoked transient and inconsistent vomiting which was also prevented by nalorphine. It is apparent, therefore, that morphinomimetic brain peptides are involved in at least two functions in the central nervous system: beta-endorphin subserves the mediation of a long-lasting psychomotor stimulation, while the enkephalins mediate vomiting of a transient character.
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PMID:Differences in central effects of beta-endorphin and enkephalins: beta-endorphin. A potent psychomotor stimulant. 627 57

The effect on behavior of synthetic human beta-Endorphin injected into the cerebral ventricles of the cat was investigated in these experiments. beta-endorphin produced psychomotor excitation (i.e., restlessness, apprehension, flight and locomotion), accompanied by pupillary dilatation and tremor. Between periods of locomotion, the cat sat moving its head from side to side with eyes wide open and mydriasis, or stood stiffly with a vacant stare, pupils dilated and eyes wide open. During this time the cat did not react to objects moving in front of it. Behavioral changes produced by a single dose of beta-endorphin were dose-dependent and long-lasting. Pretreatment with intracerebroventricular nalorphine depressed or abolished the behavioral changes, mydriasis and tremor caused by beta-endorphin. It is concluded that beta-endorphin acts on central opiate receptors promoting psychomotor excitation.
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PMID:beta-Endorphin-induced psychomotor excitation in the cat. 628 17

beta-Endorphin injected into the cerebral ventricles of unanesthetized cats produced dose-dependent and long-lasting restlessness, locomotion, stereotyped sideways movements of the head, vacant staring, apprehension and flight accompanied with mydriasis and tremor. The most impressive features of the psychomotor excitation were the locomotion and the sideways movements of the head. Intracerebroventricular nalorphine prevented the psychomotor excitation caused by intracerebroventricular beta-endorphin. Lithium chloride and lithium carbonate injected into the cerebral ventricles prevented and reversed the psychomotor excitation evoked by beta-endorphin similarly injected. In cats showing spontaneous locomotor activity, intracerebroventricular lithium chloride also suppressed this activity. It is suggested that beta-endorphin elicited psychomotor excitation by acting on central opiate receptors. However, the effect of lithium cannot be solely ascribed to an action on central opiate receptors and endogenous peptides. Since lithium affected the spontaneous as well as the beta-endorphin-induced locomotion, it may be supposed that the cation suppressed the ongoing input activity at central locomotion activity levels.
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PMID:Inhibition by lithium of beta-endorphin-induced psychomotor excitation in cats. 629 36

It was found in our earlier experiments that infusion of beta-endorphin (beta-End) into the 3rd brain ventricle in sheep elicited a differential effect on the secretion of cortisol under physiological and stress conditions. Under physiological conditions it elevated the level of cortisol in the peripheral blood, while in stressed animals it suppressed it. To obtain further support for the suppressive action of beta-End on cortisol secretion under stress conditions a beta-End antiserum was infused into the 3rd ventricle of the brain in stressed and nonstressed sheep and the concentration of plasma cortisol was measured. Stress was induced by mild electric foot shock. Infusion of the beta-End antiserum during stimulation enhanced the plasma cortisol values, when compared with those obtained during the infusion of rabbit hyperimmune serum containing anti-guinea pig gamma-globulins or saline. Moreover, during the infusion of beta-End anti-serum some aggravation of stress symptoms expressed by the increase of restlessness and higher frequency of defecations and urinations was observed. Additional experiments carried out to study the effect of beta-End on prolactin (PRL) secretion showed that this opioid induced a very high secretion of PRL in stressed animals. On the basis of these data and the known suppressive action of PRL on the corticosterone response to stress in the rat, we suggest that the suppressive action of beta-End on cortisol secretion in stressed sheep could be caused by the action of PRL.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enhancing effect of intracerebrally infused beta-endorphin antiserum on the secretion of cortisol in foot-shocked sheep. 847 8

A combined anterior pituitary (CAP) function test was assessed in eight healthy male beagle dogs. The CAP test consisted of sequential 30-second intravenous administrations of four hypothalamic releasing hormones in the following order and doses: 1 microgram of corticotropin-releasing hormone (CRH)/kg, 1 microgram of growth hormone-releasing hormone (GHRH)/kg, 10 micrograms of gonadotropin-releasing hormone (GnRH)/kg, and 10 micrograms of thyrotropin-releasing hormone (TRH)/kg. Plasma samples were assayed for adrenocorticotropin, cortisol, GH, luteinizing hormone (LH), and prolactin (PRL) at multiple times for 120 min after injection. Each releasing hormone was also administered separately in the same dose to the same eight dogs in order to investigate any interactions between the releasing hormones in the combined function test. Compared with separate administration, the combined administration of these four hypothalamic releasing hormones caused no apparent inhibition or synergism with respect to the responses to CRH, GHRH, and TRH. The combined administration of these four hypothalamic releasing hormones caused a 50% attenuation in LH response compared with the LH response to single GnRH administration. The side effects of the combined test were confined to restlessness and nausea in three dogs, which disappeared within minutes after the administration of the releasing hormones. It is concluded that with the rapid sequential administration of four hypothalamic releasing hormones (CRH, GHRH, GnRH, and TRH), the adenohypophyseal responses are similar to those occurring with the single administration of these secretagogues, with the exception of the LH response, which is lower in the CAP test than after single GnRH administration.
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PMID:Assessment of a combined anterior pituitary function test in beagle dogs: rapid sequential intravenous administration of four hypothalamic releasing hormones. 866 4


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