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 potential effect of intracerebroventricular (icv) alpha N-acetyl human beta-endorphin-(1-31) on morphine dependence was examined in mice and rats. Animals were rendered tolerant-dependent by subcutaneous (sc) implantation of an oily suspension (10 ml/Kg mouse and 3 ml/Kg rat) containing 0.1 g/ml of morphine. After 72 h of chronic morphine, 1 mg/Kg sc naloxone precipitated in both species a withdrawal syndrome that was moderate in animals pretreated with the acetylated derivative of beta-endorphin. Doses of 28 fmols/rat or 80 fmols/mouse alpha N-acetyl human beta-endorphin-(1-31) reduced the number of animals presenting the jumping behaviour, as well as the number of jumps recorded. Moreover, less than half of the rats presented the other withdrawal signs evaluated: squeak on touch, diarrhoea, chattering, chewing, ptosis and body shakes. This activity could be observed when alpha N-acetyl human beta-endorphin was injected 1 h to 24 h before naloxone; longer intervals resulted in a significant loss of this activity. The alpha 2 agonist clonidine given icv at pmol-nmol doses decreased the incidence of morphine withdrawal syndrome. Combinations of these two substances generally did not produce any further enhancement of the effects of clonidine and alpha N-acetyl beta-endorphin when used alone. Icv injections of the antagonist of alpha 2-adrenoceptors yohimbine prevented both clonidine and alpha N-acetyl beta-endorphin-(1-31) from reducing the jumping behaviour displayed by morphine-abstinent mice. It is suggested that alpha N-acetyl beta-endorphin produces this alleviation of the morphine withdrawal syndrome by improving the efficiency of alpha 2-mediated agonist effects after acting on a neural substrate that is distinct from the mu opioid receptor binding site.
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PMID:alpha N-acetyl human beta-endorphin-(1-31) alleviates the morphine withdrawal syndrome in rodents: a comparative study with clonidine. 160 92

Spastic colon is a pathological entity whose clinical symptoms are for the most part abdominal pain, constipation and episodes of diarrhea without loss of weight. In all probability, it is merely a particularly striking presentation of a GI tract that is irritable throughout its entirety. The pathophysiological basis is a disordered propulsive bowel motoricity. Etiologically, psychological factors in the presence of an appropriate genetic or acquired disposition are conceivable. Possible mediators are considered to be noradrenalin, beta-endorphin and the corticotropin-releasing factor. The diagnosis can be established with a high degree of probability on the basis of the characteristic clinical picture. A definitive diagnosis, however, requires the very careful exclusion of other possible diagnoses. Therapy includes talks with the patient, physical and dietetic measures and the use of drugs to ameliorate diarrhea or, in the case of prokinetic agents, to re-establish normal propulsive bowel activity.
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PMID:[Spastic colon (irritable colon)]. 252 95

A yin-yang hypothesis is presented linking noradrenergic activity, thromboxane, melatonin, left hemisphere functioning, and cyclic AMP on the one hand, and dopamine, beta-endorphin, calcium, right hemisphere functioning, and cyclic GMP on the other. It is further suggested that there is a yoking of NA, TXA2, serotonin and melatonin in the left hemisphere, and a similar yoking of DA, BE, calcium and cGMP in the right. Evidence is presented to support the hypothesis that each element (NA, TXA2, etc.) on one side can modulate or balance a corresponding element (DA, BE, etc.) on the other. It is suggested that thromboxane is the key element in noradrenergic overactivity and that not taking this into consideration has confounded much prior research. This theory takes into account information processing models as well as pharmacological data and neurochemical theory on coupling of adenylate cyclase to its hormone receptors. Inhibiting noradrenergic overactivity can be obtained by inhibiting thromboxane and concomitantly activating opiate receptors. This protocol may have clinical utility in treating a wide range of disorders such as: anxiety, depression, schizophrenia, sleeplessness, withdrawal states, enuresis, Gilles de la Tourette syndrome, Parkinsonism, Alzheimers, dementia, anorexia, infant ruminations, essential tremor, spasticity of spinal cord injury, diarrhoea, ulcerative colitis, extrapyramidal symptoms, akathisia, neuroleptic malignant syndrome, attention deficit disorder, hyperhidrosis, and possibly AIDS.
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PMID:Inhibiting noradrenergic overactivity by inhibition of thromboxane and concomitant activation of opiate receptors via dietary means. 254 22

A 65-year-old woman presenting with back pain, difficulties in walking and watery diarrhea. A right adrenal tumor and high excretion of catecholamines were found. Laboratory examinations showed raised levels of vasoactive intestinal polypeptide, pancreatic polypeptide, gastrin and calcitonin. Histology showed a combined pheochromocytoma-ganglioneuroma. The neoplastic cell population was immunohistochemically shown to contain tyrosine hydroxylase, neuropeptide Y, met-enkephalin, substance P, vasoactive intestinal polypeptide, calcitonin and calcitonin gene-related peptide. Postoperatively, the patient recovered fully and the hormone levels returned to normal.
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PMID:Adrenal pheochromocytoma-ganglioneuroma producing catecholamines and various neuropeptides. 318 92

Opiates and opioid peptides can alter gastrointestinal motility and delay transit of intraluminal contents. These experiments were designed to characterize the effects of beta-endorphin and [D-Ala2,Met5]enkephalinamide (DALA) on small intestinal transit in the rat. Rats were implanted with a polyethylene cannula in the right lateral cerebral ventricle and a silastic cannula in the proximal duodenum. Drugs were administered via the cerebral cannula or intraperitoneally (i.p.) Interstitial transit was assessed by instilling radiochromium into the duodenum and calculating the geometric center of the distribution of marker in the small intestine. beta-Endorphin and DALA produced a dose-related decrease in intestinal transit when the peptides were given intracerebroventricularly (i.c.v.) however, neither peptide was effective when i.p. [D-Ala2,Leu5]enkephalinamide and dynorphin-(1-13) did not alter intestinal transit. The inhibitory effects of beta-endorphin and DALA were antagonized by pretreatment with naloxone or naltrexone. A quaternary amine containing opiate antagonist. N,N-diallylnormorphinium given i.p. did not alter the response to either peptide but was effective in blocking the antitransit effects of i.p. loperamide, a peripherally acting opioid agonist. In addition, DALA reduced the body weight loss produced by castor oil-induced diarrhea while beta-endorphin had no effect. These results indicate that opioid peptides can alter intestinal motility by an action within the central nervous system. While DALA and beta-endorphin produce quantitatively the same effects on small intestinal motility, qualitatively they may differ in their mechanisms of action.
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PMID:Opioid peptides inhibit intestinal transit in the rat by a central mechanism. 612 82

General pharmacological effects of the human corticotropin-releasing hormone, corticorelin (human) (CAS 86784-80-7), on the central nervous system, somatic nervous system, autonomic nervous system and smooth muscle, respiratory and circulatory system, digestive system and miscellaneous organs were investigated. 1. The central nervous system: Corticorelin (human) had little effect on hexobarbital-induced sleeping-time, maximal electroshock-induced convulsion, acetic acid-induced writhing, rota-rod performance. Corticorelin (human) at doses of more than 10 micrograms/kg i.v. induced flush of skin and pilo-erection, at doses of more than 30 micrograms/kg i.v. decreased body temperature, delayed expression of perphenazine-induced catalepsy and indicated hunched posture, and at the dose of 100 micrograms/kg i.v. induced the rise of awake-level and decrease of the total power of EEG, and decreased the spontaneous motor activity. 2. The somatic nervous system: Corticorelin (human) did not cause muscle relaxation in mice and had little effect on neuromuscular transmission in rats. No local anesthetic activity of corticorelin (human) was exhibited through inhibition of the corneal reflex in guinea pigs. 3. The autonomic nervous system and smooth muscle: Corticorelin (human) had no effect on the contraction of isolated ileum of guinea pigs induced by histamine and acetylcholine, and on the contraction of isolated trachea of guinea pigs induced by histamine, and the pupil diameter of rabbits. Corticorelin (human) at doses more than 30 micrograms/kg i.v. decreased spontaneous motility and contractile force of uterus of non-pregnant rabbits. 4. The respiratory and circulatory system: Corticorelin (human) had no effect on the contraction of isolated aorta of rats induced by norepinephrine. Corticorelin (human) at doses of more than 3 micrograms/kg i.v. decreased the blood pressure, increased heart rates and slightly increased the number of respiration in dogs. However, corticorelin (human) had no effect on ECG and femoral blood flow in dogs. 5. The digestive system: Corticorelin (human) at doses of more than 0.3 microgram/kg i.v. increased duodenal motility and contractile force, at doses of more than 1 microgram/kg i.v. increased colonic contractile force transiently and increased antral motility. Corticorelin (human) at doses of more than 3 micrograms/kg i.v. caused diarrhea and at doses of more than 30 micrograms/kg i.v. inhibited small intestinal propulsion in mice. Corticorelin (human) at dose of 100 micrograms/kg i.v. showed an inhibition of the gastric juice secretion and decreased the excretion of Na+, Cl- and H+ in rats. Corticorelin (human) produced slight gastric damages only at the highest dose of 100 micrograms/kg i.v.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:General pharmacological properties of the human corticotropin-releasing hormone corticorelin (human). 805 70

We present two patients with manifest acquired immunodeficiency syndrome (AIDS) suffering from a generalized cytomegalovirus (CMV) infection. Over the course of several weeks they had developed a state of increasing lethargy and fatigue and one patient had noticed a darkening of his skin. These and other symptoms (vomiting, diarrhoea, hypotension) were suggestive of adrenal insufficiency. Laboratory findings included an increase of serum potassium levels, a decrease of serum sodium concentrations and elevated levels of the adrenocorticotropic hormone (ACTH). These findings, as well as the prompt therapeutic response to hydrocortisone established the diagnosis of adrenal insufficiency. Although definitive proof is lacking, generalised CMV infection is the most likely cause of our patients' symptoms. For the early initiation of appropriate substitution therapy, persons infected with the human immunodeficiency virus (HIV) with signs of CMV infection should be carefully and repeatedly monitored for clinical and laboratory signs of adrenal insufficiency.
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PMID:Primary adrenal insufficiency in two patients with the acquired immunodeficiency syndrome associated with disseminated cytomegaloviral infection. 940 82

A 3-day-old female Pinto was admitted with profuse watery diarrhea and severe hypovolemic shock. After 1 week of intensive care, the foal developed seizures associated with profound serum electrolyte abnormalities suggestive of hypoadrenocorticism. Treatment with prednisone and isotonic saline (0.9% NaCl) solution led to prompt clinical response. Premature withdrawal of prednisone resulted in relapse of clinical signs. A diagnosis of adrenal insufficiency was made on the basis of clinical signs, electrolyte abnormalities, low baseline cortisol concentration, and lack of response to administration of exogenous adrenocorticotropin. Two months later, adrenocortical function was normal and the foal was doing well clinically. Clinical signs of acute adrenal insufficiency in neonatal foals can be confused with other conditions, such as septicemia, enteritis, and ruptured urinary bladder. A persistently low serum sodium-to-potassium ratio associated with CNS malfunction should warrant investigation of adrenal gland function. Acute hypoadrenocorticism in foals may be reversible.
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PMID:Adrenal insufficiency in a neonatal foal. 960 31

Endogenous opioid peptides - enkephalins, beta-endorphin and dynorphins - are located in specific sites of the brain, the spinal cord, the autonomic ganglia and the enteric nervous system. Endogenous opioids participate in the regulation of nervous visceral afference and sensitivity as well as of several visceral motor function induced by the central nervous system and through the enteroenteric and the myoenteric reflexes. Their final effect on gut physiology is the net and harmonically balanced result of their binding to mu, delta and kappa opioid receptor subtypes. Exogenous opioid receptor ligands with different affinities for the opioid receptor subtypes have been effectively used to modify and normalize altered gut functions. The mu receptor agonists - morphine and, to a greater extent, the meperidine congeners diphenoxylate and loperamide - have been shown to slow gastrointestinal transit by their effects on the circular and longitudinal muscle of the intestine. Diphenoxylate and, more efficiently, loperamide, for the lack of any effect on the central nervous system, have been usefully employed in the treatment of diarrhea in irritable bowel syndrome (IBS) patients. Unlike the mu receptor agonists morphine and loperamide, which invariably stimulate colonic motility, trimebutine, which has almost equal affinity for mu, delta and kappa receptors, has no effect on normal colonic activity but reduces the abnormal increase in postprandial motor activity in IBS patients and accelerates slow large bowel transit in constipated patients. Opioid ligands can be usefully employed to normalize altered visceral sensitivity in IBS patients. The kappa receptor agonist fedotozine exerts its antinociceptive effect by acting on peripheral nerve endings of sensory vagal and nonvagal afferent pathways. Fedotozine has been shown to increase the threshold of perception to colonic distension in experimental conditions and to affect favourably symptoms of IBS in clinical trials.
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PMID:Role of opioid ligands in the irritable bowel syndrome. 1020 12

Ginseng is the root of the perennial herbs of Panax quinquefolium and Panax ginseng which contain a series of tetracyclic triterpenoid saponins (ginsenosides) as active ingredients. It is considered a tonic or adaptogenic that enhances physical performance (including sexual), promotes vitality and increases resistance to stress and ageing. The adaptogenic properties of ginseng are believed to be due to its effects on hypothalamic-pituitary-adrenal axis, resulting in elevated plasma corticotropin and corticosteroids levels. When used appropriately, ginseng appears to be safe. Nevertheless, documented side effects include hypertension, diarrhoea, restlessness, mastalgia and vaginal bleeding.
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PMID:The aphrodisiac and adaptogenic properties of ginseng. 1093 Jul 6


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