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)

Breakdown of the blood aqueous barrier in the rabbit eye induces a protein leakage into the aqueous humor, seen as a flare in the anterior chamber. A barrier damage was induced by topical prostaglandin E2(PGE2), infrared irradiation of the iris, or alpha-melanocyte-stimulating hormone (alpha-MSH) given subcutaneously. The aqueous flare was measured quantitatively by means of a photoelectric instrument. The interference of adrenergic antagonists and agonists on the breakdown of the barrier was tested. The alpha-adrenergic antagonist phentolamine and the beta-adrenergic antagonist propranolol, given intravenously, had no effect on exogenously administered PGE2, but both antagonists reduced the flare response to infrared irradiation which is supposed to exert its effect via endogenous prostaglandin release. The alpha-MSH response was unaffected by phentolamine, whereas propranolol abolished the flare response to alpha-MSH totally. The PGE1 response was unaffected both by the alpha-adrenergic agonist noradrenaline and the beta-adrenergic agonist terbutalin sulfate, administered topically. Noradrenaline, however, inhibited the flare response to infrared irradiation and facilitated the flare response to alpha-MSH. Terbutalin sulfate worked synergistically with both infrared irradiation and alpha-MSH. It is assumed that alpha-MSH exerts its effect on the barrier via enhanced beta-adrenergic activity, whereas the effects caused by infrared irradiation seem conditioned by intact alpha- as well as beta-adrnergic receptor sites.
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PMID:Interaction of adrenergic agents with alpha-melanocyte-stimulating hormone and infrared irradiation of the iris in the rabbit eye. 19 23

The effects of prostaglandins E on the concentration of cyclic AMP (cAMP) and a possible antagonism of opiates vs. prostaglandins E were studied in homogenates and in slices of rat striata in vitro. In homogenates, PGE1 or PGE2 did not affect the synthesis of cAMP. Morphine slightly lowered the cAMP synthesis, in presence or absence of PGE1 or PGE2. In slices, PGE2 significantly elevated the cAMP concentrations, either in presence or in absence of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine. Morphine, met-enkephalin and levorphanol, but not dextrorphan, antagonized this rise of cAMP. The effect of morphine was antagonized by naloxone. Adenosine or an elevation of K+-ions raised the cAMP concentrations, and PGE2 induced a further increase. In presence of elevated K+-ions or adenosine, however, morphine did not antagonize the PGE2-induced rise of cAMP concentration. It is suggested that under some experimental conditions described in the literature, endogenous activators of cAMP formation, e.g. adenosine, might mask the inhibitory effect of opiates on stimulation of opiates on stimulation of cAMP synthesis induced by prostaglandins E.
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PMID:Interactions of opiates and prostaglandins E with regard to cyclic AMP in striatal tissue of rats in vitro. 20 43

The aqueous flare (AF) of an intact rabbit eye was measured by a photoelectrical instrument and the intraocular pressure by vibration tonometry. Prior treatment with imidazole given intraperitoneally noticeably inhibited the disruption of the blood-aqueous barrier in rabbit eyes induced by topical prostaglandin E2 (PGE)2, topical arachidonic acid (AA), infrared irradiation of the iris, endotoxin of Proteus mirabilis given intravenously, and alpha-melanocyte-stimulating hormone (alpha-MSH) given subcutaneously. Prior treatment with imidazole given topically had no effect on the disruption of the blood aqueous barrier caused by topical PGE2, topical AA, infrared irradiation of the iris, or endotoxin of P. mirabilis given intravenously, but facilitated and potentiated strongly the response to alpha-MSH given subcutaneously. Prior treatment with topical imidazole did not affect the histological changes of the anterior ciliary processes induced by alpha-MSH given subcutaneously.
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PMID:The effect of imidazole on the disruption of the blood-aqueous barrier in the rabbit eye. 77 Mar 85

The effects of beta-endorphin, Met-enkephalin, dynorphin and SKF 10047 on the constancy of the isometric developed tension (IDT) of the spontaneous contractions of uterine strips isolated from ovariectomized rats were explored. beta-endorphin (10(-6) M) was the only opioid that depressed significantly uterine constancy of IDT in a concentration dependent fashion. Naloxone, neither at 10(-8) M nor at 10(-6) M, altered the negative inotropic influence of beta-endorphin. Moreover, the basal synthesis and outputs of some prostaglandins (PGE1, PGE2 and PGF2 alpha) from rat uteri and the effect of beta-endorphin (10(-6) M), were determined. It was found that the basal synthesis and release of PGs in uteri were significantly inhibited by this endogenous opioid. The effects of beta-endorphin (10(-8), 10(-6) and 10(-5) M) on the basal; and oxytocin or A23187, induced 45Ca2+ uptake, as well as the influence of naloxone were also studied. beta-endorphin at three of the concentrations tested decreased basal uterine 45Ca2+ uptake and this action was not prevented by naloxone (10(-8) M). The presence of oxytocin and of A23187 augmented significantly 45Ca2+ uptake, an effect that was antagonized by beta-endorphin (10(-6) M). The possible role of beta-endorphin in uterine functioning via the modulation of uterine PG synthesis and Ca2+ uptake is discussed.
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PMID:Effects of beta-endorphin on spontaneous uterine contractions. Prostaglandins production and 45Ca2+ uptake in uterine strips from ovariectomized rats. 135 70

Topical dynorphin and beta-endorphin produce increases in both prostanoid and vasopressin concentrations in cortical periarachnoid fluid of newborn pigs. The present study, in anesthetized piglets with cranial windows implanted, investigated the role of these prostanoids in the mediation of this vasopressin release by opioids. Topical prostaglandin (PG) I2 (100 ng/ml) increased pial arteriolar diameter from 145 +/- 4 to 178 +/- 4 microns and also increased cerebrospinal fluid (CSF) vasopressin from 1.1 +/- 0.1 to 4.1 +/- 0.5 microU/ml, but CSF vasopressin was not changed by PGE2, PGF2 alpha, and U-46619. Therefore, it is possible that PGI2 causes the increase in CSF vasopressin produced by opioids. Consistent with this concept, indomethacin and aspirin blocked dynorphin- and beta-endorphin-induced vasopressin release. The present data indicate that PGI2 contributes to opioid-induced changes in CSF vasopressin concentration and, thereby, to vasopressinergic contributions to opioid-induced cerebral vascular responses.
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PMID:Prostanoids modulate opioid-induced increases in cerebrospinal fluid vasopressin concentration. 148 93

Injection of a low concentration (0.3 micrograms/kg iv) of interleukin-1 beta (IL-1 beta) produced monophasic fever, but high concentrations (15 micrograms/kg iv) produced biphasic fever in rats. Treatment with IL-1 beta caused dose-dependent rises in the plasma concentration of adrenocorticotropic hormone (ACTH) 30 min after injection. Moreover, significant increases in plasma levels of ACTH were observed 90 and 180 min after injection of the high dose of IL-1 beta. ACTH response induced by IL-1 beta (15 micrograms/kg iv) was suppressed by pretreatment with injection of indomethacin (Indo), a potent inhibitor of prostaglandin (PG) synthesis, in a dose-dependent manner (1 and 10 mg/kg iv). Also, biphasic fever induced by the high dose of IL-1 beta was completely abolished by pretreatment with the intravenous injection of Indo. Intracerebroventricular (icv) injection of Indo (50 micrograms) did not affect febrile and ACTH responses induced by intravenous IL-1 beta, whereas those responses induced by IL-1 beta (2 ng icv) were significantly suppressed by injection of Indo (50 micrograms icv). Although it is possible that intracerebroventricular Indo does not reach the site of intravenous IL-1 beta action within the brain, these results suggest that in rats febrile and ACTH responses induced by intravenous IL-1 beta are caused by IL-1 beta-acting structures outside the blood-brain barrier. It is likely that these structures subsequently synthesize and release PGE2, which in turn induces ACTH and febrile responses in rats.
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PMID:ACTH response in rats during biphasic fever induced by interleukin-1. 165 33

Interleukin 1 alpha (IL-1 alpha), a powerful endogenous pyrogen released from monocytes and macrophages by bacterial endotoxin, stimulates corticotropin, prolactin, and somatotropin release and inhibits thyrotropin release by hypothalamic action. We injected recombinant human IL-1 alpha into the third cerebral ventricle, to study its effect on the pulsatile release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) in conscious, freely moving, ovariectomized rats. Intraventricular injection of 0.25 pmol of IL-1 alpha caused an almost immediate reduction of plasma LH concentration; this decrease was statistically significant 20 min after injection and occurred through a highly significant reduction in the number of LH pulses, with no effect on pulse amplitude. In contrast, there was no change in pulse frequency but a small significant elevation in amplitude of FSH pulses. Intraventricular injection of the diluent had no effect on gonadotropin release. The results provide further evidence for separate hypothalamic control mechanisms for FSH and LH release. To determine the mechanism of the suppression of LH release, mediobasal hypothalamic fragments were incubated in vitro with IL-1 alpha (10 pM) and the release of LH-releasing hormone (LHRH) and prostaglandin E2 into the medium was measured by RIA in the presence or absence of norepinephrine (50 microM). IL-1 alpha reduced basal LHRH release and blocked LHRH release induced by norepinephrine. It had no effect on the basal release of prostaglandin E2; however, it completely inhibited the release of PGE2 evoked by norepinephrine. To evaluate the possibility that IL-1 alpha might also interfere with the epoxygenase pathway of arachidonic acid metabolism, epoxyeicosatrienoic acids were also measured. IL-1 alpha had no effect on the content of epoxyeicosatrienoic acids in the hypothalamic fragments as measured by gas chromatography and mass spectrometry. In conclusion, IL-1 alpha suppresses LH but not FSH release by an almost complete cessation of pulsatile release of LH in the castrated rat. The mechanism of this effect appears to be by inhibition of prostaglandin E2-mediated release of LHRH.
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PMID:Interleukin 1 alpha inhibits prostaglandin E2 release to suppress pulsatile release of luteinizing hormone but not follicle-stimulating hormone. 190 15

The influences of opioids on pial arteriolar diameter and cortical periarachnoid cerebrospinal fluid prostanoid concentration were investigated in piglets with closed cranial windows. Methionine enkephalin (10(-12)-10(-6) M) increased pial arteriolar diameter (139 +/- 4, 149 +/- 3, 178 +/- 3 microns, for control, 10(-12), and 10(-6) M, respectively). Leucine enkephalin produced similar pial arteriolar dilation. In contrast, dynorphin elicited dilation during normotension and constriction during hypotension. beta-Endorphin (10(-12)-10(-6) M) decreased pial arteriolar diameter (137 +/- 6, 128 +/- 6, 92 +/- 7 microns, for control, 10(-12) and 10(-6) M, respectively). All four opioids increased cerebrospinal fluid 6-keto-prostaglandin (PG)F1 alpha, PGE2, PGF2 alpha and thromboxane B2. Indomethacin (5 mg/kg i.v.) blocked methionine and leucine enkephalin and dynorphin-induced pial arteriolar dilation, but potentiated beta-endorphin-induced constriction and the constriction caused by dynorphin in hypotensive piglets. These data indicate that prostanoids modulate opioid effects on the cerebral vasculature.
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PMID:Prostanoids modulate opioid cerebrovascular responses in newborn pigs. 197 12

The role of melanocyte stimulating hormone (MSH) as a mediator of the melanogenic response to ultraviolet radiation (UVR) was examined in C57 BL/6 mice. While exposure to UVR (250-300 nm) for 7, 14 and 27 days increased tyrosinase activity in epidermal melanocytes of the ear MSH had no effect and failed to alter the response to UVR. Plasma alpha-MSH concentrations were unchanged following UVR. Theophylline, a phosphodiesterase inhibitor, also had no effect on epidermal tyrosinase activity in non-irradiated and UV irradiated mice. Prostaglandin E2 and arachidonic acid were also ineffective in non-irradiated and UV irradiated mice and indomethacin, an inhibitor of prostaglandin synthesis, failed to increase epidermal tyrosinase activity after UVR. On the other hand, 12-0-tetradecanoyl phorbol 13 acetate, an activator of protein kinase C, increased epidermal tyrosinase activity in non-irradiated mice and also enhanced the effect of UVR.
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PMID:The effect of ultraviolet radiation and melanocyte-stimulating hormone on tyrosinase activity in epidermal melanocytes of the mouse. 212 69

We have examined the possibility that corticotropin-releasing hormone (CRH) and adrenocorticotropin (ACTH) might affect prostaglandin (PG) E2 and PGF2 alpha output by term placenta, amnion and decidua during short-term (48-hour) culture, and that effects of CRH might be mediated by ACTH. In all three tissues PG output was stimulated by both CRH and ACTH. These effects were inhibited in the presence of antisera to CRH and to ACTH. Moreover, in placenta, but not in amnion or decidua, the stimulatory effects of CRH on PGE2 and PGF2 alpha output were attenuated in the presence of an antibody to ACTH. Our results support the possibility of paracrine stimulation by CRH and ACTH of PG production in intrauterine tissues, and suggest that in part the effects of CRH on placental PG output might be mediated through ACTH.
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PMID:Effects of corticotropin-releasing hormone and adrenocorticotropin on prostaglandin output by human placenta and fetal membranes. 216 98


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