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)

Small infusions of strong acid create large elevations in heart rate (HR), mean arterial pressure (MAP), adrenocorticotropic hormone (ACTH), cortisol, and thromboxane A2 (TxA2). We hypothesized that TxA2 is responsible for these hormonal and hemodynamic responses. Conscious sheep received HCl (1 N, 1 ml/min for 30 min) with or without receiving SQ-29548 [a TxA2/prostaglandin (PG) H2 receptor antagonist]. HCl increased TxB2 from 133 +/- 44 to 1,213 +/- 531 (SE) pg/ml while SQ-29548 + HCl increased TxB2 from 141 +/- 41 to 1,051 +/- 518 pg/ml. HCl decreased pH (7.464 +/- 0.015 to 7.413 +/- 0.011), arterial PCO2 (31.6 +/- 1.3 to 25.9 +/- 1.8 mmHg), and arterial PO2 (98.0 +/- 2.2 to 90.5 +/- 3.2 mmHg), and increased MAP (75 +/- 2 to 88 +/- 5 mmHg), HR (72 +/- 4 to 93 +/- 8 beats/min), hematocrit (25 +/- 1 to 29 +/- 2%), ACTH (154 +/- 41 to 549 +/- 217 pg/ml), and aldosterone (25 +/- 1 to 151 +/- 74 pg/ml) while these responses were prevented by SQ-29548. SQ-29548 reduced but did not prevent the cortisol response to HCl (9 +/- 2 to 23 +/- 10 ng/ml compared with 6 +/- 2 to 17 +/- 4 pg/ml after SQ-29548). K+ and aldosterone also increased after the end of SQ-29548 + HCl treatment (4.0 +/- 0.1 to 4.5 +/- 0.1 meq/l and 53 +/- 21 to 147 +/- 61 pg/ml, respectively). We conclude that TxA2 mediates the blood gas, MAP, HR, ACTH, and aldosterone responses to HCl infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thromboxane A2 receptor antagonism prevents hormonal and cardiovascular responses to mineral acid infusion. 797 50

In 6 cats, mean +/- SEM baseline plasma concentrations of cortisol, corticotropin, and alpha-melanocyte-stimulating hormone (alpha-MSH) were 87 +/- 16 nmol/L, 73 +/- 14 ng/L, and 129 +/- 12 ng/L, respectively. The cats were subjected to: handling and subsequent skin testing without anesthesia; anesthesia with 50 mg of ketamine HCl and 2.5 mg of diazepam given IV, immediately followed by handling and skin testing; and anesthesia and handling as previously described, but without skin testing. Significant (P < 0.05; multivariate analysis for repeated measures) increase in plasma cortisol, corticotropin, and alpha-MSH concentrations was observed until 20 minutes after the start of the experiments in cats undergoing physical restraint and subsequent skin testing with or without preceding anesthesia. These responses were largely abolished when anesthesia with ketamine and diazepam was only followed by handling. We conclude that, during stress in cats (in contrast to dogs), the pituitary intermediate lobe is activated to secrete alpha-MSH. In addition, the cortisol response after skin testing of cats under anesthesia may be a reasonable explanation for the reported weak skin test reactivity in cats.
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PMID:Changes in plasma cortisol, corticotropin, and alpha-melanocyte-stimulating hormone concentrations in cats before and after physical restraint and intradermal testing. 838 Dec 60

Mineral acid infusion is used to investigate the effects of acidemia on the cardiovascular and respiratory systems. Previous studies have shown that small infusions of HCl increase mean arterial pressure (MAP), adrenocorticotropic hormone (ACTH), and cortisol without producing acidemia. We infused 1 meq/min of 1 N HCl intravenously into chronically catheterized conscious sheep with or without pretreatment with 1.1 mg/kg flunixin-N-methylglucamine, a cyclooxygenase inhibitor (n = 6). Acid infusion resulted in significant increases in heart rate (83 +/- 5 to 94 +/- 7 beats/min), MAP (84 +/- 3 to 104 +/- 6 mmHg), ACTH (97 +/- 23 to 285 +/- 101 pg/ml), cortisol (20 +/- 3 to 37 +/- 16 ng/ml), sodium (149.5 +/- 0.8 to 150.6 +/- 1.3 meq/l), potassium (3.96 +/- 0.09 to 4.31 +/- 0.19 meq/l), and thromboxane (Tx) B2 (stable metabolite of TxA2) (147 +/- 78 to 2,304 +/- 1,213 pg/ml), whereas these changes were prevented by flunixin. Plasma concentrations of 6-ketoprostaglandin F1 alpha (stable metabolite of prostacyclin), prostaglandin E2, interleukin-1 alpha, and hematocrit did not change in either group. Arterial pH decreased, whereas arterial partial pressure of CO2 increased significantly in both groups. Arterial partial pressure of O2 declined in both groups, but the decrease was significantly greater in the group not receiving flunixin. We conclude that a cyclooxygenase metabolite, most likely TxA2, mediates the MAP, heart rate, ACTH, and cortisol responses to mineral acid infusion.
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PMID:Prostanoid cascade inhibition prevents cardiovascular and adrenocorticotropic responses to mineral acid infusion. 839 58

Various endocrine responses to 5-hydroxytryptamine (serotonin, 5-HT) agonists were used to assess serotonergic receptor function after chronic treatment with the antidepressants fluoxetine (10 mg/kg), a 5-HT uptake blocker and the norepinephrine uptake blocker desipramine (DMI, 5 mg/kg). Both were injected (i.p.) once a day for 21 days. DOI (5-HT1C/2 agonist, 0-5 mg/kg i.p.) and 6-chloro-2-[1-piperazinyl]-pyrazine (MK-212) (less selective, but predominantly a 5-HT1C agonist, 0-20 mg/kg i.p.) were administered 18 hr after the final antidepressant injection and 30 min before decapitation. Chronic treatment with both fluoxetine and DMI produced a potentiation in most hormone responses to the 5-HT agonists (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-amino-propane HCl (DOI) and MK-212, although there were several differences in individual hormone responses to the two 5-HT agonists. Fluoxetine and DMI potentiated the MK-212- and DOI-induced increase of plasma oxytocin levels and potentiated the effect of DOI on plasma adrenocorticotropic hormone (corticotropin) and prolactin levels. In contrast, the effect of the high dose of MK-212 on plasma prolactin concentration was reduced by both antidepressants. Only MK-212 increased vasopressin levels and this effect was potentiated by fluoxetine, but not by DMI. Fluoxetine also significantly increased the resting level of plasma vasopressin. DMI potentiated the effect of MK-212 on plasma renin concentration. Pretreatment with fluoxetine significantly increased (38%) the Bmax for the 5-HT1C/2 agonist sites ([125I]DOI) in the hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term treatment with the antidepressants fluoxetine and desipramine potentiates endocrine responses to the serotonin agonists 6-chloro-2-[1-piperazinyl]-pyrazine (MK-212) and (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane HCl (DOI). 839 20

In order to elucidate the effects of MPTP on enkephalinergic neurons, dopamine (DA), norepinephrine (NE), proenkephalin (PE) mRNA and met-enkephalin (ME) were measured in striatum, olfactory tubercle, and prefrontal cortex of C57/B16 mice 1 day-2 weeks following treatment with 96 mg/kg MPTP HCl (24 mg/kg i.p., twice/day for 2 days). DA and its metabolites were depleted 70% in striatum and 40% in olfactory tubercle within 1 day. In cortex, DA was unchanged, whereas homovanillic acid and NE were depleted 50 and 40% respectively by 3 days. ME increased in all three brain regions at different times whereas PE mRNA showed a different pattern in each region, with an increase in olfactory tubercle, a decrease in cortex, and in striatum, a decrease at 1 day followed by an increase at 3 days. Thus enkephalinergic neurons in each region respond differently to MPTP treatment. In striatum and olfactory tubercle. DA is depleted sufficiently to release its tonic inhibition on the enkephalinergic neurons, thereby leading to increased enkephalin synthesis. In cortex, the change in NE metabolism appears to cause a decrease of ME release and thereby a depression of PE synthesis. The possible relationship between these results and the changes observed in Parkinson's disease are discussed.
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PMID:1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) effects on enkephalinergic neurons in various regions of mouse brain. 843 70

We sought to evaluate the antiinflammatory effects of synthetic human beta-endorphin (SHB) when injected into the canine knee joint. Sixteen healthy dogs, aged 1-2 yr, were selected. SHB was injected pre- and postinjury into each knee. The sample size was n = 32 after a randomized factorial arrangement; 2 x 4 with four cases per treatment being performed. Factors considered were: Factor A with two levels: A1 = Preinjury and A2 = Postinjury; Factor B (SHB dose) with four levels: B1 = Control, B2 = 250 micrograms, B3 = 500 micrograms, B4 = 1000 micrograms. The control group received 0.9% NaCl solution. Anesthesia was induced with intravenous thiopental, 14 mg/kg, and acepromazine, 0.5 mg/kg. Injury was produced with an intraarticular injection of 4 mL HCl 0.5 M, which was left in situ for 20 min. Inflammation was measured using the 610 nm absorbency of Evans blue extravasate in biopsy specimens. Histopathologic studies were performed on each knee. We found that beta-endorphin has a clear, dose-related, antiinflammatory effect, reducing the tissue extravasation of Evans blue and its absorbency, especially with large doses. This finding was consistent with the histopathologic observations. We conclude that SHB has an antiinflammatory effect. It is still not clear which mechanisms inhibit polymorphonuclear cell adhesion to vascular endothelium or cell and plasmatic protein extravasation.
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PMID:An evaluation of the antiinflammatory effects of intraarticular synthetic beta-endorphin in the canine model. 871 98

Intravenous mineral acid infusions into fetal sheep stimulate increases in plasma adrenocorticotropic hormone (ACTH) and cortisol concentrations that correlate to the induced changes in arterial pH (pHa). We have recently demonstrated that ACTH and cortisol responses to mineral acid infusion in adult sheep are mediated by thromboxane A2 (TxA2). We designed the present experiments to test the hypothesis that fetal ACTH and cortisol responses are also mediated by TxA2. We infused chronically instrumented fetal sheep with 1 N HCl (0.5 ml/min i.v.) for 60 min, with or without pretreatment with the cyclooxygenase inhibitor flunixin-N-methylglucamine. HCl infusion significantly decreased pHa and significantly increased the arterial partial pressure of O2 (PaO2) and CO2 (PaCO2). Flunixin pretreatment significantly decreased fetal plasma thromboxane B2 (TxB2) concentrations but did not significantly alter the blood gas and pH response to HCl. TxB2 is a stable metabolite of TxA2 and was measured as an index of TxA2 generation. HCl increased fetal heart rate only in the flunixin group. Plasma ACTH and cortisol concentrations were increased significantly in both groups; flunixin did not significantly alter the responses. HCl infusion did not significantly alter plasma TxB2 concentrations. We conclude that the fetal ACTH and cortisol responses to HCl infusion are not mediated by TxA2 or other prostanoids whose synthesis depends on cyclooxygenase activity.
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PMID:Does thromboxane mediate the fetal ACTH response to acidemia? 878 Feb 25

Two series of experiments were conducted to investigate the role of corticotropin-releasing hormone (CRH) in the effects of 5-hydroxytryptamine (5-HT) on energy intake and energy expenditure. The first set of experiments was carried out to confirm the influence of 5-HT1A-, 5-HT1B-, 5-HT2A/2C-receptor agonists on the activation of the hypothalamic-pituitary-adrenal axis. Plasma corticosterone levels were measured, and a double-immunolabeling procedure was used to determine whether the neuronal activity marker, c-Fos protein (Fos), could be found within brain neurons containing CRH after treatments with 5-HT1A-, 5-HT1B-, 5-HT2A/2C-receptor agonists. The second series of experiments was conducted to assess the involvement of CRH in the effects of 5-HT on food intake and metabolic rate (VO2). The effects of the 5-HT1A-, 5-HT1B-, 5-HT2A/2C-receptor agonists on food intake and VO2 were measured in rats treated with the CRH antagonist, alpha-helical CRH-(9-41). In both experiments rats were intraperitoneally injected with either a vehicle (NaCl 0.9%), the 5-HT1A-receptor agonist (+/-)-8-hydroxy-2-(di-n-propylamino) tetralin hydrobromide (8-OH-DPAT), the 5-HT1B-receptor agonist 5-methoxy-3-(1,2,3,6-tetrahydro-4-pyridinyl)-1H-indole succinate (RU-24969), or the 5-HT2A/2C-receptor agonist (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane HCl (DOI). Fos immunoreactivity was detectable within the CRH-containing neurons of the paraventricular nucleus of the hypothalamus (PVH) after injection of each of the 5-HT-receptor agonists used. The CRH antagonist alpha-helical CRH-(9-41) attenuated the increases in metabolic rate induced by DOI and 8-OH-DPAT. alpha-Helical CRH did not, however, prevent the effects of RU-24969 and DOI on either nocturnal metabolic rate or food intake. The present results provide further evidence for a role of CRH in 5-HT-mediated thermogenic effect, which likely involves the 5-HT2A/2C receptor during the day and the 5-HT1A receptor during the night. Moreover, these results do not support a role for CRH in 5-HT anorectic effects, which likely involves 5-HT1B and 5-HT2A/2C receptors. Finally, the results of this study indicate that the stimulation of CRH-containing neurons located in the PVH does not necessarily predict changes in food intake and energy expenditure.
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PMID:Role of CRH in the effects of 5-HT-receptor agonists on food intake and metabolic rate. 894 58

We examined the effect of urocortin (Ucn) on the adrenocorticotropin (ACTH) release from cultured rat anterior pituitary cells and AtT 20 cells. Synthetic rat (r)Ucn was not soluble in 0.1 N HCl but soluble in alkaline solvents with diminished corticotropin-releasing activity. rUcn dissolved in 0.1 M sodium phosphate buffer as a stock solution maintained its bioactivity and had the equal corticotropin-releasing activity with rat/human corticotropin-releasing factor (r/hCRF). rUcn stimulated the adrenocorticotropin release via CRF-receptors accompanied by the additive effect with r/hCRF, the synergistic effect with arginine vasopressin and the dose-dependent inhibition of a potent CRF-receptor antagonist.
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PMID:Effect of urocortin and its interaction with adrenocorticotropin (ACTH) secretagogues on ACTH release. 953 39

Differential adaptive changes in serotonin2A [5-hydroxytryptamine (5-HT)2A] receptor signaling during treatment may be one mechanism involved in the latency of therapeutic improvement with antidepressants, such as fluoxetine. We examined the effects of fluoxetine (2, 3, 7, 21, or 42 days) on hypothalamic 5-HT2A receptor signaling. The hormone responses to an injection of the 5-HT2A receptor agonist (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-amino-propane HCl (DOI) were used as an index of hypothalamic 5-HT2A receptor function. Treatment with fluoxetine for 21 or 42 days produced diminished adrenocorticotropic hormone (ACTH) and oxytocin (but not corticosterone) responses to DOI injections (2.5 mg/kg i.p.; 15 min postinjection). Regulators of G protein signaling 4 and Galphaq protein levels in the hypothalamic paraventricular nucleus were not altered during fluoxetine treatment. Because previous studies indicate that treatment with fluoxetine for 21 days resulted in increased hormone responses to DOI when measured at 30 min after injection, we examined the effect of fluoxetine (21 days) on DOI-induced increase hormone levels at 15, 30, and 60 min after DOI injection. Fluoxetine decreased the oxytocin response at 15 but not at 30 min post-DOI injection, and potentiated the ACTH and corticosterone responses at 30 min post-DOI injection. For comparison, we examined the effect of fluoxetine on 5-HT2A receptor-mediated increase in phospholipase C (PLC) activity in the frontal cortex. 5-HT-stimulated, but not guanosine 5'-O-(3-thio)triphosphate-stimulated PLC activity was increased after 21 days of fluoxetine-treatment. Overall, these results indicate that chronic fluoxetine treatment can potentiate 5-HT2A receptor signaling in frontal cortex but differentially alters 5-HT2A receptor signaling in oxytocin-containing neurons and corticotropin-releasing factor-containing neurons in the paraventricular nucleus.
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PMID:Chronic fluoxetine differentially affects 5-hydroxytryptamine (2A) receptor signaling in frontal cortex, oxytocin- and corticotropin-releasing factor-containing neurons in rat paraventricular nucleus. 1272 28


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