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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We hypothesized that augmented responses of glucoregulatory hormones in iron deficiency would enhance liver and muscle glycogenolysis, leading to increased gluconeogenic precursor (lactate) supply and upregulation of hepatic gluconeogenesis. Female weanling rats were randomly placed on either a mildly iron-deficient (-Fe; 15 mg Fe/kg diet) or an iron-sufficient (+Fe; 50 mg Fe/kg diet) diet for 4 wk and studied at rest and during exhaustive treadmill running. Hemoglobin was 9.0 +/- 0.2 and 13.1 +/- 0.3 g/dl in -Fe and +Fe, respectively, after 3.5 wk of dietary iron deficiency. Arterial plasma epinephrine (Epi), norepinephrine (NE), adrenocorticotropic hormone (ACTH), corticosterone, insulin, and glucagon levels were similar at rest in both groups, as were liver, gastrocnemius, and superficial and deep vastus medialis glycogen levels. Liver and kidney phosphoenolpyruvate carboxykinase (PEPCK) activities were similar in both groups. Maximum O2 consumption was decreased (22%) in -Fe. Respiratory exchange ratio (CO2 production/O2 consumption) was unaffected at rest but increased at maximum O2 consumption in -Fe. Time to exhaustion during a standardized running test (13.4 m/min, 0% grade) was decreased 45% in -Fe (63 +/- 5 vs. 116 +/- 10 min). During exercise, euglycemia was maintained in both groups, but blood lactate was elevated in -Fe. The mean net glycogen utilization during exercise was increased in liver (43%), soleus (33%), and superficial vastus medialis (106%) and decreased in the gastrocnemius (36%) in -Fe. Liver and kidney PEPCK activities were increased similarly at exhaustion in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Augmented glucoregulatory hormone concentrations during exhausting exercise in mildly iron-deficient rats. 823 58

An attempt was made to determine sex differences in the effects of beta-endorphin (beta-EP) on respiratory and cardiovascular systems using Wistar rats. By the intracerebroventricular administration of beta-EP (0.18 mg/kg) to normal male and female rats, respiratory rate (RR), heart rate (HR) and mean arterial blood pressure (MABP) were depressed significantly (p < 0.01 or 0.001) and CO2 in expired gas increased significantly (p < 0.01). These suppressive effects of the peptide were transiently blocked by the intravenous injection of naloxone (0.2 mg/kg). No differences in the effects of beta-EP between estrous and diestrous female rats could be detected. The effects of the peptide were significantly stronger in RR, HR and MABP for females than for males (0.001 < p < 0.05). Testectomized rats showed suppressive effects of the peptide to the same extent as intact females, but the effects in ovariectomized rats did not differ from those for intact females. In testectomized and ovariectomized rats treated with testosterone, the former showed the same results as intact males, but not the latter. The suppressive effects of beta-EP on the respiratory and cardiovascular systems are thus remarkably relieved by androgen in male rats.
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PMID:Sex differences in respiratory and cardiovascular effects of beta-endorphin. 834 81

Previous studies have demonstrated that fetal adrenocorticotropic hormone (ACTH) and arginine vasopressin (AVP) are increased during periods of acidemia produced by infusion of acid intravenously or by acidemia secondary to hypovolemia. The purpose of this study was to quantify ACTH and AVP responses to hypercapnic acidemia and to test the role of the peripheral chemoreceptors in the control of these responses. Chronically catheterized fetal sheep were subjected to carotid sinus denervation and bilateral vagotomy or were studied intact. At least 5 days after surgery, fetuses were exposed to a 60-min period of normocapnia or hypercapnia, delivered via a polyethylene bag containing 5-8% CO2 in 21% O2 fitted over the head of the pregnant ewe. Hypercapnia significantly increased fetal arterial PCO2 to 55.2 +/- 1.8 and 55.9 +/- 2.2 mmHg and decreased arterial pH to 7.257 +/- 0.011 and 7.281 +/- 0.010 in intact and denervated fetuses, respectively. Fetal mean arterial blood pressure was decreased slightly in the denervated fetuses during hypercapnia. Fetal plasma AVP was increased in both groups equally, and plasma ACTH and cortisol were increased in the denervated fetuses only. Fetal heart rate was increased significantly in intact but not denervated fetuses. We conclude that respiratory acidemia is a mild stimulus to AVP secretion and that this response is not attenuated by peripheral chemodenervation.
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PMID:The adrenocorticotropic hormone and arginine vasopressin responses to hypercapnia in fetal and maternal sheep. 838 63

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

We have investigated the regulatory role of nitric oxide (NO) in corticotropin-releasing hormone (CRH) release from the human perfused placental lobule in vitro. The effects of the NO donor sodium nitroprusside, the NO synthase inhibitor N omega-nitro-L-arginine, and the NO substrate L-arginine on human (h) placental CRH secretion have been studied. Single lobules of term placentae were bilaterally perfused with Krebs solution (5 mL/min; 95% O2-5% CO2; 37 C; pH 7.3). Fetal and maternal perfusates were collected at 4 C every 30 min for 3 h. CRH immunoreactivity (CRH-IR) in perfusates was measured by RIA using the 41-residue synthetic CRH as standard, 125I-labeled Tyr-hCRH as tracer, and a rabbit anti-CRH antibody Y2BO. The sensitivity of the assay was 0.13 pmol/L. Under basal conditions, human perfused placentae in vitro continuously secreted CRH-IR, which diluted in parallel to a synthetic hCRH-(1-41) standard curve. Size-exclusion chromatography of placental perfusates using a Sephadex G-50 column indicated that placental CRH-IR predominately coeluted with hCRH-(1-41) standard. Basal maternal perfusate CRH-IR levels (27 +/- 4 pmol/L) released from perfused placental lobules were nearly 10-fold greater than fetal perfusate CRH-IR levels (3.4 +/- 0.7 pmol/L; P < 0.05). Infusion of sodium nitroprusside (30-100 mumol/L) into the maternal and fetal placental circulations inhibited CRH-IR release into maternal perfusate in a concentration-dependent manner, but did not inhibit CRH-IR release into the fetal perfusate. N omega-nitro-L-arginine (100 mumol/L) increased placental CRH-IR secretion into fetal perfusate, and this effect was reversed by the infusion of L-arginine (100 mumol/L), which also reduced release below basal levels. In contrast, maternal perfusate CRH-IR levels were not affected by N omega-nitro-L-arginine or L-arginine. These results indicate that the human perfused placenta in vitro releases a substance of similar mol wt and hCRH-IR. Moreover, modulators of the NO signaling pathway differentially affect placental secretion of CRH-IR into the maternal and fetal perfusates. These data are consistent with the involvement of NO in the regulation of placental CRH release during pregnancy.
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PMID:Nitric oxide regulation of corticotropin-releasing hormone release from the human perfused placenta in vitro. 863 1

Heme oxygenase is an essential enzyme in the heme catabolism that produces carbon monoxide (CO). This study was designed to examine the expression of two heme oxygenase isozyme mRNAs in the human brain and to explore the involvement of nitric oxide (NO) and various neuropeptides in the regulation of their expression. Northern blot analysis showed the expression of heme oxygenase-1 and heme oxygenase-2 mRNAs in every region of the brain examined, with the highest levels found in the frontal cortex, temporal cortex, occipital cortex, and hypothalamus. In a human glioblastoma cell line, T98G, treatment with any of three types of NO donors--sodium nitroprusside, 3-morpholinosydnonimine, and S-nitroso-L-glutathione--caused a significant increase in the levels of heme oxygenase-1 mRNA but not in the levels of heme oxygenase-2 and heat-shock protein 70 mRNAs. Sodium nitroprusside increased the levels of heme oxygenase-1 protein but not the levels of heat-shock protein 70 in T98G cells. The increase in content of heme oxygenase-1 mRNA caused by sodium nitro-prusside was completely abolished by the treatment with actinomycin D. On the other hand, the levels of heme oxygenase isozyme mRNAs were not noticeably changed in T98G cells following the treatment with 8-bromo cyclic, GMP sodium nitrite, or various neuropeptides, such as calcitonin gene-related peptide, endothelin-1, and corticotropin-releasing hormone. The present study has shown the expression profiles of heme oxygenase-1 and -2 mRNAs in the human brain and the induction of heme oxygenase-1 mRNA caused by NO donors in T98G cells. These findings raise a possibility that the CO/heme oxygenase system may function in concert with the NO/NO synthase system in the brain.
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PMID:Expression of heme oxygenase isozyme mRNAs in the human brain and induction of heme oxygenase-1 by nitric oxide donors. 876 71

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

Neuroendrocrine and substrate responses were investigated in eight male athletes during inhalation of either 100% O2 (HE), 14% O2 (HO) or normoxio gas (NO) before, during and after 60 min of cycle ergometry at the same absolute work rate. Concentrations of prolactin (PRL), growth hormone (GH), testosterone (T), adrenocorticotropic hormone (ACTH), cortisol (COR), adrenalin (A), noradrenalin (NA), insulin (INS), ammonia (NH3), free fatty acids, serotonin (5-HT), total protein, branched-chain amino acids (BCAA) and free tryptophan (free TRP) were determined in venous blood and lactate concentration [LA-], partial pressure of oxygen (PO2), oxygen saturation (SO2), partial pressure of carbon dioxide and pH in capillary blood. The PO2 and SO2 were augmented in HE and decreased in HO (P < or = 0.01). In HO and NO no significant changes were found for any other parameter during 30 min of rest prior to exercise. In HE, PRL increased by about 400% during this time, while NA declined (P < or = 0.01). Heart rate (HR) and [LA-] were higher during exercise in HO (P < or = 0.01). In all trials, NH3, NA, A, T, GH and ACTH increased during exercise (P < or = 0.01), while BCAA and INS declined. In comparison to NO and HE, increases of NA, A, GH, COR and ACTH were higher in HO (P < or = 0.01). The PRL in NO and COR in NO and HE did not change significantly. In HE, after the initial increase at rest, PRL declined during exercise but remained higher than in HO. Higher values for NA, A, GH, COR and ACTH in HO were likely to have reflected an augmented relative exercise intensity. Our results showed that PRL but no other hormone increased during acute exposure to hyperoxia. This PRL release was independent of exercise stress and greater than PRL augmentation during hypoxia, which was related to a higher relative exercise intensity as indicated by [LA-] and HR. Responses of plasma NH3, BCAA, free TRP and 5-HT could not explain PRL augmentation induced by the increment in blood SO2 during hyperoxia.
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PMID:Effect of O2 availability on neuroendocrine variables at rest and during exercise: O2 breathing increases plasma prolactin. 895 92

Human corticotropin-releasing hormone (hCRH) and thyrotropin-releasing hormone (TRH) are known to stimulate ventilation after i.v. administration in humans. In a placebo-controlled, single-blind study we aimed to clarify if both peptides act by altering central chemosensitivity. Two subsequent CO2-rebreathing tests were performed in healthy young volunteers. During the first test 0.9% NaCl was given i.v.; during the second test 200 micrograms of hCRH (n = 12) or 400 micrograms of TRH (n = 6) was administered i.v. Nine subjects received 0.9% NaCl i.v. during both rebreathing manoeuvres. The CO2-response curves for the two tests were compared within the same subject. In the hCRH group a marked parallel shift of the CO2-response curve to the left was observed after hCRH (P < 0.01). The same effect occurred following TRH but was less striking (P = 0.05). hCRH and TRH caused a reduction in the CO2 threshold. The CO2-response curves in the control group were nearly identical. The results indicate an additive effect of both releasing hormones on the hypercapnic ventilatory response in humans, presumably independent of central chemosensitivity.
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PMID:Human corticotropin-releasing hormone and thyrotropin-releasing hormone modulate the hypercapnic ventilatory response in humans. 895 5

Little is known about the effect of alpha-MSH and other melanogenic stimulators on avian melanocytes. Tissue cultures of Barred Plymouth Rock regenerating feather melanocytes were established and the culture medium contained selected concentrations of alpha-MSH and other melanogenic stimulators in Ham's F-10 medium supplemented with antibiotics and 10% new born calf serum. Cultures were maintained at 37 degrees C in 95% air/5% CO2. No increase in melanogenesis over control levels due to the addition of 10(-5) M Forskolin, 10(-4) M IBMX, 10(-3) M c-GMP, and 10(-3) M db-c-AMP was observed in the cultures on days 5 and 7. However, 2.5 (optimum), 5, and 10 micrograms/ml alpha-MSH and 10(-3) M 8-bromo-c-AMP significantly increased melanogenesis over control levels on days 5 and 7. The stimulation of melanogenesis was detectable by a significantly increased number of melanocytes containing numerous stage IV melanosomes. No increase in melanocyte cell number was observed in any of the experimental cultures. The addition of 1, 2 (optimum), or 3 mM calcium did enhance the increased pigmentation effect of 2.5 micrograms/ml alpha-MSH. Two very convincing experiments showed that c-AMP was the second messenger for alpha-MSH in these birds. First, the c-AMP inhibitor, 10(-3) M Rp-c-AMPS, completely inhibited the stimulatory effect of alpha-MSH in these in vitro melanocytes. Second, direct measurements of c-AMP levels in feather tissue showed a significant increase in c-AMP levels 10.min after alpha-MSH treatment. Controls received no alpha-MSH. The results showed that these avian melanocytes have alpha-MSH receptors and were able to respond to the hormone. C-AMP was the second messenger in this system. Apparently db-c-AMP was not able to enter these mature, highly-differentiated cells and c-AMP agonists, Forskolin and IBMX, were also either unable to enter these older cells or, if they did enter the cells, were unable to stimulate c-AMP production. Evidently the more lipophilic 8-bromo-c-AMP was able to enter these cells and stimulate melanogenesis.
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PMID:The role of alpha-MSH, its agonists, and C-AMP in in vitro avian melanocytes. 917 Jan 61


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