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)

Histamine (HA) stimulates the release of the pro-opiomelanocortin (POMC)-derived peptides ACTH, beta-endorphin (beta-END), beta-lipotropin and alpha-melanocyte-stimulating hormone, and HA is involved in the mediation of the stress-induced release of these peptides. The effect of HA is indirect and may involve the hypothalamic regulating factors, corticotropin-releasing hormone (CRH) and/or arginine-vasopressin (AVP). We studied the effect of immunoneutralization with specific antisera against CRH or AVP on the response of ACTH and beta-END to HA, restraint stress, CRH, AVP or a posterior pituitary extract in male rats. Intracerebroventricular infusion of HA (34-540 nmol) increased the plasma levels of ACTH and beta-END immunoreactivity (beta-ENDir) in a dose-dependent manner. Pretreatment with antiserum to CRH or AVP prevented the ACTH response to 270 nmol HA and inhibited the beta-ENDir response by 30-60%. One to five minutes of restraint stress caused an increase in the plasma levels of ACTH and beta-ENDir. The increase was dependent on the duration of stress exposure. Pretreatment with CRH antiserum abolished the ACTH response to 5 min of restraint stress and inhibited the beta-ENDir response by 60%. Immunoneutralization with AVP antiserum had only half the inhibitory effect of that seen with CRH antiserum. CRH (100 pmol i.v.) increased the plasma levels of ACTH and beta-ENDir. This effect was abolished by pretreatment with CRH antiserum, whereas pretreatment with AVP antiserum prevented the CRH-induced ACTH release and inhibited the beta-ENDir response by 50%. AVP (24-800 pmol i.v.) stimulated ACTH and beta-ENDir in a dose-dependent manner. CRH and AVP antisera each prevented the effect of AVP (800 pmol) on ACTH secretion, whereas the beta-ENDir response to AVP was only inhibited by about 60% by the antisera. An extract of the posterior pituitary gland administered in a dose corresponding to 0.15 or 0.5 pituitary equivalents had no effect on ACTH secretion, while 1.0 pituitary equivalent increased the ACTH concentration in plasma. This effect was abolished by AVP antiserum. The posterior pituitary extract caused a dose-dependent rise in plasma beta-ENDir which might be due to an unavoidable contamination of the posterior pituitary extract by a small amount of beta-END from the intermediate lobe. Consistent with this view, AVP antiserum had no effect on the rise in the plasma concentration of beta-ENDir following administration of the posterior pituitary extract.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Histamine- and stress-induced secretion of ACTH and beta-endorphin: involvement of corticotropin-releasing hormone and vasopressin. 133 40

Histamine (HA) stimulates the release of adrenocorticotropic hormone (ACTH) and beta-endorphin (beta-END) via activation of central postsynaptic H1 or H2 receptors. The effect of HA is indirect and may involve the hypothalamic regulating factors corticotropin-releasing hormone (CRH), arginine vasopressin, or oxytocin (OT). We studied the effect of specific HA H1 or H2 receptor agonists on the concentration of CRH and OT in hypophyseal portal blood in urethane-anesthetized male rats. In addition we investigated the effect of the agonists on ACTH and beta-END immunoreactivity in peripheral plasma in conscious male rats pretreated with antiserum to CRH. Intracerebroventricular administration of the H1 receptor agonist 2-thiazolylethylamine (2-TEA) or the H2 receptor agonist 4-methylhistamine (4-MeHA) increased the CRH concentration in pituitary portal blood by 80-90% when compared to preinfusion levels (p < 0.05). Central infusion of saline had no effect. The level of OT in the pituitary portal blood was not affected by 2-TEA or 4-MeHA when compared to saline-treated rats. Intracerebroventricular infusion of 2-TEA or 4-MeHA increased the ACTH concentration in peripheral plasma 3- or 4-fold, respectively (p < 0.01). Pretreatment with a specific CRH antiserum (abCRH) inhibited the responses by 50 and 70%, respectively (p < 0.01). Intracerebroventricular administration of 2-TEA or 4-MeHA increased the beta-END immunoreactivity in peripheral plasma 3- or 2-fold, respectively (p < 0.01). These effects were inhibited by 80-90%, when rats were pretreated with abCRH (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Histamine H1 and H2 receptor activation stimulates ACTH and beta-endorphin secretion by increasing corticotropin-releasing hormone in the hypophyseal portal blood. 136 94

The use of antisense peptides for receptor isolation as proposed by Blalock and his colleagues (e.g. TIBTECH 8, 140-144, 1990) was tested for human ACTH as well as alpha- and beta-MSH. We synthesized the corresponding antisense peptides HTCAh, HSM-alpha and HSM-beta and analyzed them for specific interaction with the sense peptides using several types of binding assay and bioassay. Similarly HTCAh antibodies were tested for binding to ACTH receptors and ACTH antibodies. All these experiments were negative, i.e. there was no specific interaction between sense and antisense peptides nor between the corresponding antibodies. Receptor binding of the sense peptides was not affected by the antisense peptides or HTCAh antibodies. Unexpectedly, HTCAh but not HSM-alpha or HSM-beta was a weak MSH agonist acting through a site independent of the MSH receptor. A detailed analysis of the concept of antisense peptides revealed that the theoretical background of the hypothesis of the 'molecular recognition theory' is rather weak, explaining the failure of various attempts to obtain specific receptor antibodies.
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PMID:Antisense peptides: tools for receptor isolation? Lack of antisense MSH and ACTH to interact with their sense peptides and to induce receptor-specific antibodies. 165 31

The neurotransmitter histamine participates in the neuroendocrine regulation of pituitary hormone secretion by an indirect action at a hypothalamic level where histaminergic neurons are abundant. The effect of histamine is caused by activation of postsynaptic H1- or H2-receptors. Histamine stimulates the secretion of ACTH, beta-endorphin (mediated by CRH and AVP), alpha-MSH (mediated by dopamine and peripheral catecholamines), and PRL (mediated by dopamine, serotonin and AVP), and participates in the stress-induced release of these hormones and possibly in the suckling- and estrogen-induced PRL release. The release of GH and TSH is predominantly inhibited by histamine; however, uncertainty exists regarding its role and the hypothalamic factors involved. Histamine increases the secretion of LH in females (mediated by GnRH), and may be involved in the mediation of the estrogen-induced LH surge. AVP and oxytocin are stimulated by histamine, probably by an effect in the supraoptic and paraventricular nuclei of the hypothalamus.
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PMID:The role of histamine in the neuroendocrine regulation of pituitary hormone secretion. 206 91

A human foreskin organ culture system has been developed to study the response of human skin to hormonal stimulation. Foreskins are maintained in culture on floating plastic supports which allows the epidermal surface to be exposed to air while the dermis is bathed in nutrient medium. Both black and white human foreskins can be maintained in organ culture for at least 1 wk with no change in the tissue structure or cell viability as determined by histochemical staining and by dopa reaction staining. Tyrosinase activity in both black and white human foreskin cultures decays markedly during the first 2 d of culture to a new steady state level which remains stable throughout the culture period. Both black and white foreskin cultures consistently demonstrate 2- to 10-fold increases in tyrosinase activity when treated with theophylline (1 mM). Approximately 90% of all skin cultures examined showed an increase in enzyme activity when treated with this phosphodiesterase inhibitor. Dibutyryl cAMP (0.1 mM) and [Nle4, D-phe7]-alpha MSH (10(-8) M), were also found to markedly stimulate tyrosinase activity in some skin cultures, whereas alpha-MSH and prostaglandin E1 produced only an inconsistent and small increase in the activity of the enzyme. Histamine (1 microM), vitamin D3 (1 microM), and retinoic acid (1 microM) failed to stimulate tyrosinase activity in either white or black foreskin cultures. This hormone-responsive organ culture system can be utilized to characterize the molecular processes responsible for the regulation of tyrosinase and pigmentation in human skin.
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PMID:Hormonal stimulation of tyrosinase activity in human foreskin organ cultures. 216 16

Histamine (HA), which acts as a neurotransmitter in the central nervous system, participates in the neuroendocrine regulation of prolactin (PRL) secretion. HA has a predominant stimulatory effect which is mediated via H2-receptors following central administration and via H1-receptors following systemic infusion of the amine. In addition, HA seems to exert a minor inhibitory effect on PRL secretion, an effect unmasked only during blockade of the receptor mediating the stimulatory effect. Following central administration the inhibitory effect is mediated via H1-receptors, while following systemic administration this effect is mediated via H2-receptors. In accordance with these findings, the H2-receptor antagonist cimetidine (CIM) has an inhibitory (following central administration) or stimulatory (following systemic administration) effect on PRL secretion. However, high doses of CIM possess an additional PRL stimulatory action not related to blockade of H2-receptors. This non-specific action is not exerted by the chemically different H2-receptor antagonist ranitidine. Since HA has no effect directly at the pituitary level, the actions of the amine may occur at different sites within the hypothalamus by an effect on hypothalamic transmitters regulating PRL secretion. Dopaminergic as well as serotoninergic neurons are involved in the mediation of the action of HA, since the dopamine (DA) concentration in the pituitary portal vessels is decreased by central or systemic infusion of HA, and since blockade of DA synthesis and of DA or serotonin (5-HT) receptors inhibit or prevent the PRL stimulatory action of HA infused centrally or systemically. However, other factors regulating PRL secretion (e.g. beta-endorphin, vasoactive intestinal peptide, vasopressin or TRH) may be involved in the mediation of the PRL response to HA. In men the effects of HA on PRL secretion are similar to the effects in male rats. Systemic infusion of HA stimulates PRL secretion via H1-receptors and inhibits PRL secretion via H2-receptors. The PRL-stimulatory effect of HA is caused by an inhibition of the dopaminergic system, while the PRL-inhibitory effect of HA may involve other transmitters than DA. In contrast to its stimulatory effect in men, HA had no effect on basal PRL secretion in women, but enhanced the PRL response to TRH. In rats or in humans the PRL stimulatory effect of HA is not caused by the cardiovascular actions of the amine.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Histaminergic regulation of prolactin secretion. 218 99

Histamine, which acts as a neurotransmitter, stimulates the release of the pro-opiomelanocortin derived peptides ACTH, beta-lipotropin, and beta-endorphin. Since stress affects the hypothalamic turn-over of neuronal histamine, we investigated the role of histaminergic neurons in the mediation of the stress-induced release of ACTH and beta-endorphin immunoreactivity in male rats. In control animals histamine receptor antagonists had no effect on the release of ACTH or beta-endorphin immunoreactivity. Restraint and ether stress increased plasma ACTH 3- and 2-fold, respectively. The responses were almost prevented by intracerebroventricular or intra-arterial infusion of the H2-receptor antagonists cimetidine and ranitidine. Infused intracerebroventricularly the H1-receptor antagonist mepyramine inhibited the ACTH response to restraint by 45% (P less than 0.01), but had no effect on the response to ether. Infused intra-arterially the H1-receptor antagonists mepyramine or SKF-93944 had no effect. Restraint and ether stress increased plasma beta-endorphin immunoreactivity 6- and 5-fold, respectively. Sephadex G-50 gel chromatography of plasma showed that the beta-endorphin immunoreactivity in stressed rats co-eluted with beta-lipotropin and beta-endorphin, whereas the immunoreactivity in control animals co-eluted almost exclusively with beta-endorphin. The H2-receptor antagonists cimetidine and ranitidine infused intracerebroventricularly inhibited the responses of beta-endorphin immunoreactivity to restraint and ether stress by 90 and 70%, respectively, whereas intra-arterial infusion of these antagonists inhibited the responses by only 50 and 60%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Involvement of histaminergic neurons in the stress-induced release of pro-opiomelanocortin-derived peptides in rats. 256 49

The effect of histamine on the release of beta-endorphin-like immunoreactivity (beta-END LI) in rats was studied in vivo and in vitro experiments. Intravenous injection of 100 micrograms/100g BW of histamine resulted in a significant increase in the plasma beta-END-LI level 5, 15 minutes after the injection. Histamine at concentrations of 10(-12) to 10(-9)M also caused dose-dependent stimulation of release of beta-END-LI from the dispersed cells of the anterior pituitary of rats. On gel-chromatography, the beta-END-LI released by incubating the cells with 10(-9)M histamine consisted of two components, which eluted in the same positions as human beta-lipotropin and human endorphin, respectively. Addition of 2mM CoCl2 to the incubation medium inhibited histamine-induced beta-END LI release from the cells. Histamine H1 receptor antagonist (10(-6)M) inhibited histamine-induced beta-END-LI release from the cells. Histamine H2 receptor antagonist (10(-6)M), however, did not inhibit histamine-induced beta-END-LI release. These results indicate that histamine acts directly on the anterior pituitary cells to stimulate beta-END-LI 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 histamine on the release of beta-endorphin-like immunoreactivity]. 287 89

The effect of histamine and related compounds on the plasma beta-endorphin-like immunoreactivity (beta-En-Li) levels in rats were studied. Histamine (2.5 mg/kg), mepyramine (10 mg/kg) or famotidine (5.0 mg/kg) was injected i.p., and the animals were serially decapitated. The plasma beta-En-Li levels were measured by radioimmunoassay. Effects of histamine, mepyramine and famotidine on beta-En-LI release from the anterior pituitary were also investigated by means of an in vitro experiment. The beta-En-LI content in the hypothalamus and pituitary gland did not change significantly after histamine, mepyramine and famotidine injection. The plasma beta-En-LI levels increased significantly in a dose-related manner with a zenith at 20 min after histamine injection and decreased significantly after mepyramine injection, but did not change significantly after famotidine injection. Effects of histamine on plasma beta-En-LI levels were prevented with the pretreatment of mepyramine. The beta-En-LI release from the anterior pituitary was enhanced with the addition of histamine to the medium, and histamine's effects were blocked with an addition of mepyramine to the medium. These findings suggest that histamine acts as to stimulate beta-En-LI release from the anterior pituitary, and that histamine's effects may be mediated via H1-receptor.
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PMID:Effect of histamine and its blockers on plasma beta-endorphin-like immunoreactivity in rats. 295 84

The antihistaminic activity of many antidepressant drugs is well documented in vitro but has not been investigated as thoroughly in vivo. In the course of an investigation of the roles of H1 and H2 receptors in histamine-induced adrenocorticotropic hormone (ACTH) release in rats, it was observed that several antidepressants were potent inhibitors of this response. Male Sprague-Dawley rats were injected with test drugs and then with histamine or histamine agonists. Serum ACTH concentrations were determined by radioimmunoassay. ACTH secretion was induced by both H1 and H2 receptor stimulation. Histamine-induced ACTH release was markedly attenuated by several H1 antihistamines, whereas the H2 antagonists were not as effective. The antidepressants imipramine, doxepin, mianserin, desipramine and amitriptyline suppressed histamine-induced ACTH release. However, iprindole and the antianxiety agent diazepam were without effect. ACTH release induced by histamine agonists was also diminished by pretreatment with some of these blocking agents.
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PMID:Suppression of histamine-induced adrenocorticotropic hormone release by antihistamines and antidepressants. 612 82


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