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)

Cholecystokinin octapeptide (CCK-8) stimulated adrenocorticotropin hormone (ACTH) release from both rat anterior pituitary cells in culture and a tumor cell line of the mouse anterior pituitary (AtT-20/D16-16). The stimulation of ACTH release was dependent on the time of exposure to CCK-8 and the concentration of this peptide applied to anterior pituitary cells. Cerulein evoked ACTH release whereas human gastrin 1, CCK-4 and desulfated CCK-8 only produced minimal affects on ACTH release at concentrations of 10(-4) M. In contrast, these latter three peptides were as effective as CCK-8 in inducing the secretion of amylase from pancreatic acinar cells. Antagonists of CCK-8 receptors in the pancreas such as proglumide, benzotript and dibutyryl cyclic GMP did not affect the ACTH release response to CCK-8. The CCK-8 stimulation of ACTH release was calcium-dependent and blocked by glucocorticoid pretreatment. The mechanisms by which CCK-8 evoked ACTH release appears distinct from that of other ACTH secretagogues such as corticotropin releasing factor and vasopressin. The data suggest that CCK-8 is a corticotropin releasing factor-like agent acting through a putative novel receptor subtype in the anterior pituitary.
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PMID:Cholecystokinin-8 stimulates adrenocorticotropin release from anterior pituitary cells. 241 42

Behavioral effects of cholecystokinin (CCK) were observed in neofrontal decorticated and sham-operated rats. In the decorticated rats the cataleptic and analgesic effects of beta-endorphin were markedly enhanced. When CCK-antiserum was administered together with beta-endorphin, these effects were also enhanced. Sulfated CCK-8 decreased locomotion and rearing in open field test. Proglumide, a selective antagonist of CCK, blocked CCK-8-induced-hypomotility, but it had no influence on the actions of CCK-4. When general activity was monitored using an Automex, the activity counts markedly increased in the decorticated rats, while in the sham-operated rats such increase was not observed. Non-sulfated CCK-8 also stimulated the motility, particularly in the decorticated rats. On the other hand, CCK-4 was opposite to the results of CCK-8. In the decorticated rats rearing, sniffing and head stereotypy were increased by CCK-8, but grooming was not affected.
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PMID:Behavioral effects of cholecystokinin and its related peptides in rats. 293 43

The effects of cholecystokinin octapeptide (CCK-8), cholecystokinin tetrapeptide amide (CCK-4), beta-endorphin, proglumide, and naloxone on passive avoidance behavior were studied in rats. Intracerebroventricular (i.c.v.) injection of beta-endorphin (1-10 micrograms) had no significant influence on the latency of the avoidance response in intact rats. Also, beta-endorphin (0.05-5 micrograms, i.c.v.) did not affect the response in rats treated with electroconvulsive shock (ECS). The preventive effect of CCK-8 (0.1-1.0 micrograms, i.c.v.) on ECS-induced amnesia was partly antagonized by beta-endorphin (0.05-10 micrograms, i.c.v.). Intraperitoneal (i.p.) injection of naloxone (1-10 mg/kg) could not prevent ECS-induced amnesia, but continuous subcutaneous infusion of this drug (2 mg/day, 7 days) completely abolished the amnesia. Naloxone (1 and 10 mg/kg, i.p.) also partly antagonized amnesia induced by proglumide (1 and 10 micrograms, i.c.v.) and prevented it when induced by CCK-4 (5 and 10 micrograms, i.c.v.). The results indicate the facilitating action of naloxone and the inhibitory effect of beta-endorphin on memory, suggesting that the endogenous opiate systems are involved in some way in the memory processes.
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PMID:Interactions of cholecystokinin, beta-endorphin, and their antagonists on passive avoidance behavior in rats. 296 63

Binding of 3H-enkephalinamide and 3H-naloxone to P2-fractions of whole rat brain homogenate displayed saturable, stereospecific binding to receptor sites with at least two binding sites for 3H-metenkephalinamide (type I: KD = 0.4 nM and Bmax = 35 fmol/mg protein; type II: KD = 5.7 nM and Bmax = 57 fmol/mg protein) and for 3H-naloxone (type I: KD = 1.5 nM and Bmax = 40 fmol/mg protein; type II: KD = 51 nM and Bmax = 255 fmol/mg protein). beta-endorphin and met- and leu-enkephalin produced a concentration-dependent inhibition of 3H-met-enkephalinamide and 3H-naloxone binding with dissociation constants in the nanomolar range, but with very different displacement curves. Purified porcine ACTH (1-39) displaced both 3H-met-enkephalinamide and 3H-naloxone with dissociation constants of 3.4 X 10(-7) M and 1.8 X 10(-6) M, respectively. The synthetic congeners, ACTH (1-32) and to a lesser extent ACTH (1-28) and ACTH (1-24) showed a similar effect, whereas other fragments of ACTH were inactive in concentrations ranging from 10(10) to 10(-6) M. In the same concentration range cholecystokinin congeners (CCK-8 and CCK-4) were without effect. Since ACTH immunoreactive nerves seem also to contain beta-endorphin and furthermore, to show a partially overlapping distribution with the enkephalinergic systems it is possible that the binding of ACTH fragments to opiate receptors is of physiological relevance.
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PMID:Interaction of putative opioid peptides with opiate receptors. 626 26

The effect of cholecystokinin octapeptide (CCK-8) on the release of beta-endorphin-like immunoreactivity (beta-EpLI) in rats was studied in vivo and in vitro. Intravenous injection of 5 micrograms/100 g body weight of CCK-8 resulted in significant increase in the plasma beta-EpLI level after 10 and 20 min. CCK-8 at concentrations of 10(-10) - 10(-6) M also caused dose-dependent stimulation of beta-EpLI release from dispersed cells of rat anterior pituitary. However, CCK-4 and desulfated CCK-8 had no effect. On gel chromatography, the beta-EpLI released by incubation of the cells with 10(-8) M CCK-8 separated into two components, eluted in the same positions as human beta-lipotropin and human beta-endorphin, respectively. CCK-8 did not stimulate beta-EpLI release in Ca++-free medium. A 23187 at concentrations of 10(-6) - 10(-3) M caused dose-dependent stimulation of beta-EpLI release from the cells. Addition of 2 X 10(-3) M CoCl2, 10(-3) M verapamil or 10(-7) M dexamethasone to the incubation medium inhibited CCK-8-induced beta-EpLI release from the cells. Dibutyryl cyclic GMP (3 X 10(-3) M) inhibited CCK-8-induced beta-EpLI release from the cells. Ouabain (10(-5) M) also stimulated beta-EpLI release but its effect was not additive with that of CCK-8. These results indicate that CCK-8 acts directly and specifically on anterior pituitary cells to stimulate beta-EpLI release and that calcium ion is involved in the mechanism of this effect.
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PMID:In vivo and in vitro effects of cholecystokinin octapeptide on the release of beta-endorphin-like immunoreactivity. 630 91

The influence of clonidine pretreatment on psychopathological, endocrine and respiratory effects of cholecystokinin tetrapeptide (CCK-4) was characterized. Patients with panic disorder (DSM-III-R) were given 50 micrograms CCK-4 i.v. at 1100 hours on 2 separate study days. In a randomized double-blind design they were additionally infused with 150 micrograms clonidine or placebo from 1040 to 1110 hours. After CCK-4 all patients experienced symptom attacks. No effects of clonidine on panic psychopathology or blood gas parameters were observed. After CCK-4, in the clonidine condition the pituitary release of adrenocorticotropin (ACTH) and prolactin was seemingly enhanced compared to placebo. Our results suggest that CCK-4-induced panic attacks are not suppressible by presynaptic alpha-2 receptor stimulation. Moreover, they point to a synergistic postsynaptic action of clonidine to CCK-4 upon pituitary hormone secretion. The diverging sites of action might possibly explain the discrepancies of psychopathological alterations and stress hormone secretion.
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PMID:Influence of clonidine on psychopathological, endocrine and respiratory effects of cholecystokinin tetrapeptide in patients with panic disorder. 933 81

Preclinical findings on the role of corticotropin releasing hormone (CRH) in stress and anxiety, on the interaction of CRH and cholecystokinin (CCK) in modulating anxiety, as well as the blunted corticotropin (ACTH) response to CRH in panic disorder suggest that CRH may play a role in panic disorder. To further characterize the role of the hypothalamic-pituitary-adrenocortical (HPA) system in panic disorder, we compared patients with and without CCK tetrapeptide (CCK-4) induced panic attacks. Twenty-four patients with panic disorder were given injections of CCK-4 (25 micrograms). Panic attacks, psychopathological changes, as well as ACTH and cortisol secretion were recorded. Fifteen of the 24 patients experienced a panic attack after CCK-4. ACTH secretion was significantly higher in the patients with CCK-4-induced panic attacks than in those without such attacks. The patients without CCK-4-induced attacks had a brief but less pronounced increase in ACTH concentrations. Cortisol concentrations were not significantly increased after CCK-4 administration. The increased ACTH concentrations suggest that the activation of the HPA system in CCK-4-induced panic attacks plays a physiological role. CRH may be involved in experimentally-occurring and perhaps in naturally-occurring panic attacks as well.
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PMID:Increased ACTH concentrations associated with cholecystokinin tetrapeptide-induced panic attacks in patients with panic disorder. 1069 52

Given the anxiogenic effects of the type-B natriuretic peptide receptor agonist C-type natriuretic peptide (CNP) in rodents, we investigated the influence of CNP pretreatment upon the behavioral and endocrine action of the panicogen cholecystokinin tetrapeptide (CCK-4) in healthy men. In a randomized double-blind balanced design, 20 male volunteers were given an intravenous infusion of 300 microg of CNP vs. placebo followed by 25 microg of CCK-4. The behavior was assessed using panic, anxiety, and dissociation questionaires before the infusion and after the CCK-4 stimulus. Furthermore, the stress-sensitive hormones adrenocorticotropic hormone (ACTH), cortisol, and prolactin were measured. CNP pretreatment enhanced the anxiogenic and prodissociative effects of CCK-4 and significantly augmented the ACTH surge after CCK-4. However, no effect of CNP was seen upon panic symptoms. Our preliminary data support a role of type-B natriuretic peptide receptors in anxiety modulation in normal man.
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PMID:Intravenous C-type natriuretic peptide augments behavioral and endocrine effects of cholecystokinin tetrapeptide in healthy men. 1175 55

The anorexigenic effect of cholecystokinin (CCK) is well documented in mammals, but documentation in neonatal chicks is limited. Thus, the present study investigated the mechanism underlying the anorexigenic effect of CCK in neonatal chicks. Intraperitoneal (IP) injection of sulfated CCK(26-33) (CCK8S) significantly decreased food intake in chicks at 60 and 300 nmol/kg. Non-sulfated CCK(26-33) (CCK8) also significantly decreased food intake, but its anorexigenic effect was observed only at the highest dose (300 nmol/kg) and short-lived. However, CCK(30-33) (CCK4) had no effect on food intake. Also, the intracerebroventricular (ICV) injection of CCK8S (0.2 and 1 nmol) significantly decreased food intake in chicks. Similar to IP administration, the anorexigenic effect of CCK8 was weak and CCK4 did not affect food intake. IP and ICV injections of CCK8S caused conditioned aversion and increased plasma corticosterone concentrations, suggesting that their anorexigenic effects might be related to stress and/or malaise. This might be true in ICV-injected CCK8S because co-injection of astressin, a corticotropin-releasing hormone receptor antagonist, tended to attenuate the effect of CCK8S. The present study revealed that N-terminal amino acids and the sulfation of Tyr are important for the anorexigenic effect of CCK8S after IP and ICV administered in chicks. Additionally, the effect of central CCK8S might be related to stress and/or malaise.
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PMID:Feeding-suppressive mechanism of sulfated cholecystokinin (26-33) in chicks. 2222 12

Intravenous cholecystokinin-tetrapeptide (CCK-4) administration reliably and dose-dependently provokes panic anxiety in man, accompanied by adrenocorticotropic hormone (ACTH) and cortisol release. Preclinical findings suggest that behavioral and endocrine effects of CCK-4 are mediated via corticotropin-releasing hormone (CRH) release. Anxiogenic stimulation of the central CCK-receptors in man was shown to increase as well vasopressin (AVP), which acts synergistically with CRH as pituitary-adrenocortical axis stimulator during stress. Copeptin (CoP), the C-terminal part of pre-pro-AVP, is released in an equimolar ratio to AVP. It is more stable in the circulation and easier to determine than AVP and it was found to closely mirror the production of AVP. So far, CoP secretion has not been characterized during panic provocation. In 30 healthy male human subjects, we repeatedly measured CoP in plasma during a panic challenge and studied its correlation to Acute Panic Inventory (API) ratings and plasma ACTH and cortisol. CoP levels correlated positively with the increase in API ratings (r=0.41, p=0.03), while ACTH or cortisol did not (r=0.08, p=0.68 and r=0.12, p=0.53, respectively). CoP levels correlated also positively with ACTH (r=0.48, p=0.009) and cortisol (r=0.48, p=0.01) concentrations throughout the CCK-4 challenge. As expected, we found a positive correlation between plasma ACTH and cortisol levels (r=0.57, p=0.001). A vasopressinergic activation during CCK-4 induced panic was demonstrated, which was correlated positively to panic symptoms and pituitary-adrenocortical release. Our findings suggest a role of CoP as a potential surrogate marker of CCK-4 panic symptoms. Further studies are needed to replicate our results and to further clarify the role of CoP as a stress-sensitive hormone in different panic paradigms as well as in panic patients.
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PMID:Copeptin - A potential endocrine surrogate marker of CCK-4-induced panic symptoms? 2787 Oct 26


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