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)

A stimulatory role for endogenous dopamine (DA) in the regulation of hypothalamo-pituitary-adrenal activity has previously been demonstrated. In the present study, the roles of D1 and D2 subtypes of DA receptors in the regulation of activity of the hypothalamo-pituitary-adrenal axis were investigated. The intraperitoneal administration of either the D1 agonist, SKF 383393 (1-phenyl-2,3,4,5 tetrahydro-(iH)-benzazepine-7,8diol HCl, 5-20 mg/kg) or the D2 agonist quinpirole (0.05-1 mg/kg) dose-dependently elevated both adrenocorticotropic hormone (ACTH) and corticosterone (CS) in serum. Similarly, administration of either SKF 38393 or quinpirole (1-100 micrograms) into the third ventricle dose-dependently elevated ACTH in serum. The response of ACTH to intraperitoneal SKF 38393 was blocked by pretreatment with the D1 antagonist SCH 23390 (1-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5 tetrahydro-1H-3-benzazepine, 0.25 mg/kg, i.p.) but not by the D2 antagonist sulpiride (50 mg/kg, i.p.). The response of ACTH to intraperitoneal injection of quinpirole was blocked by pretreatment with sulpiride and attenuated slightly by pretreatment with SCH 23390. Further, the co-administration of sub-maximum doses of SKF 38393 and quinpirole caused additive increases in ACTH in serum. These results suggest that both D1 and D2 subtypes of DA receptors contribute to the dopaminergic regulation of function of the hypothalamo-pituitary-adrenal axis and support a role for DA neurons in the hypothalamus in this response. Further, these findings suggest that the D1 and D2 receptors, mediating the response of the hypothalamopituitary-adrenal axis are not tightly coupled.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:D1 and D2 dopamine receptors stimulate hypothalamo-pituitary-adrenal activity in rats. 132 19

Angiotensin II (ANG II) and vasopressin participate in baroreflex regulation of adrenocorticotropic hormone (ACTH), glucocorticoid, and renin secretion. The purpose of this study was to determine whether this participation is enhanced in water-deprived dogs, with chronically elevated plasma ANG II and vasopressin levels, compared with water-replete dogs. The baroreflex was assessed by infusing increasing doses of nitroprusside (0.3, 0.6, 1.5, and 3.0 micrograms.kg-1.min-1) in both groups of animals. To quantitate the participation of ANG II and vasopressin, the dogs were untreated or pretreated with the competitive ANG II antagonist saralasin, a V1-vasopressin antagonist, or combined V1/V2-vasopressin antagonist, either alone or in combination. The findings were as follows. 1) Larger reflex increases in ANG II, vasopressin, and glucocorticoids, but not ACTH, were produced in water-deprived dogs compared with water-replete dogs. 2) ANG II blockade blunted the glucocorticoid and ACTH responses to hypotension in water-deprived dogs, but not water-replete dogs. In contrast, vasopressin blockade reduced the ACTH response only in water-replete dogs. 3) Vasopressin or combined vasopressin and ANG II blockade reduced the plasma level of glucocorticoids related either to the fall in arterial pressure or to the increase in plasma ACTH concentration in water-replete dogs, and this effect was enhanced in water-deprived dogs. 4) In both water-deprived and water-replete animals, saralasin and/or a V1-antagonist increased the renin response to hypotension, but a combined V1/V2-antagonist did not. These results reemphasize the importance of endogenous ANG II and vasopressin in the regulation of ACTH, glucocorticoid, and renin secretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vasopressin and angiotensin II in reflex regulation of ACTH, glucocorticoids, and renin: effect of water deprivation. 132 65

Interleukin-1 (IL-1), a cytokine produced during infection and inflammation, mediates some of the endocrinological alterations that parallel these processes. The purpose of this study was to determine whether human recombinant IL-1 (hrIL-1) affects aldosterone output as well as renin and adrenocorticotropic hormone (ACTH) release, two key factors in the regulation of mineralocorticoid secretion. We observed that intravenous administration of hrIL-1 into conscious unrestrained rats elicited a marked and rapid rise in aldosterone plasma levels in a dose-dependent manner. The hrIL-1-induced increase in aldosterone levels was associated with enhanced renin activity and increased ACTH levels in plasma. Furthermore, aldosterone levels of IL-1-injected rats were positively correlated with plasma renin activity (PRA), suggesting that the renin-angiotensin system contributes to the changes observed in the levels of the mineralocorticoid hormone. ACTH seems also to be implicated in the aldosterone response to hrIL-1 because the profile of the kinetic curves of changes in the levels of the pituitary hormone and aldosterone was similar. Pretreatment with the cyclooxygenase inhibitor indomethacin markedly reduced the increase in aldosterone plasma levels and PRA induced by IL-1, indicating that prostaglandins are involved in these effects of the cytokine. These results suggest that IL-1 may play an important role in the control of homeostasis during infectious and inflammatory diseases.
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PMID:Interleukin-1 stimulates aldosterone secretion: involvement of renin, ACTH, and prostaglandins. 132 66

This study was undertaken to define the resting pattern of fetal pituitary-adrenocortical function. Experiments were performed at 127-145 days gestation in fetal sheep with chronic peripheral and adrenal cannulas inserted under halothane anesthesia. With the fetus in a baseline state, over 6 h, at 30-min intervals, maternal and fetal peripheral samples were collected for blood gases and cortisol (F), corticosterone (B), and adrenocorticotropic hormone (ACTH) concentrations, and three successive, 2-min adrenal samples were collected for determination of F and B secretion rates. We observed high-frequency, episodic bursts of F secretion. A lower frequency oscillation of F secretion, with a period of approximately 90 min, was defined by cosinor analysis. The mean amplitude of the oscillation increased from 45 to 507 ng/min with advancing gestation. The pattern of B secretion was similar to that for F but was quantitatively lower. An oscillatory period of approximately 90 min for plasma F was present in a majority of experiments. Pulsatile rhythms for ACTH were defined in 10 of 14 experiments, with periods ranging from 1.64 h in the least mature group to 2.37 h in the oldest fetus. Mean data revealed exponential increases in both F secretion and plasma ACTH from 129 to 145 days gestation.
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PMID:Adrenal corticosteroid secretion in fetal sheep: pulsatile pattern at rest. 132 68

Corticotropin-releasing factor (CRF-41) and arginine vasopressin (AVP) are the two major factors that regulate adrenocorticotropic hormone (ACTH) secretion. The two neurohormones are co-localized in the parvocellular neurons of the paraventricular nuclei (PVN) of the hypothalamus and are capable of potentiating each others' action on freshly excised anterior pituitary fragments or cells in vitro. Transection of all axons entering the medial basal hypothalamus from anterior and lateral directions blocks ACTH release induced by either adrenalectomy or ether-surgery stress. Adrenalectomy-induced ACTH release is almost completely suppressed by a long-term lesion of the PVN. Stress-induced ACTH release is blocked for only a few days after PVN lesion and the pituitary-adrenal response to ether-surgery stress returns to a large extent by a few weeks after PVN lesioning. This remarkable plasticity can be observed also in the homozygous Brattleboro rat, therefore it is not dependent on mediation by AVP. When parvocellular CRF-41- and AVP-containing cells are present, and the anterior lobe ACTH cells are desensitized to the stimulating effects of AVP, the ACTH response to haemorrhage and immobilization is markedly decreased. This indicates that AVP may partially mediate ACTH release under normal conditions. The hypothalamic control of the pituitary-adrenocortical system has a remarkable degree of redundancy which may compensate, at least under stressful conditions, for disruption of the function of CRF-41-containing cells of the paraventricular nucleus, the major source of CRF-41 in the stalk-median eminence.
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PMID:The relative importance of hypothalamic neurons containing corticotropin-releasing factor or vasopressin in the regulation of adrenocorticotropic hormone secretion. 133 Apr 58

Acute cocaine administration alters secretion of anterior pituitary hormones in experimental animals, and cocaine abuse may compromise neuroendocrine function in humans. The goal of this study was to examine cocaine's acute effects on neuroendocrine hormones in cocaine-dependent men. Plasma adrenocorticotropic hormone (ACTH), luteinizing hormone and prolactin levels were measured in 18 men before and after i.v. administration of cocaine (30 mg) or placebo. Each subject served as his own control during the i.v. placebo and cocaine administration conditions. Plasma cocaine levels peaked at 260 ng/ml within 5 min after the i.v. injection. Plasma ACTH levels increased significantly above base-line levels at 5, 15, 30 (P < .01) and 45 min (P < .05) after i.v. cocaine. Plasma luteinizing hormone levels increased significantly above base-line levels at 5 (P < .05) and at 15 min (P < .01) after i.v. cocaine. No changes in plasma ACTH or luteinizing hormone levels were found after i.v. placebo injection. Plasma prolactin levels decreased significantly at 30, 45, 60, 90 and 120 min (P < .01) after both i.v. cocaine and placebo administration. Cocaine-induced increases in plasma ACTH levels may be due to its effects on dopaminergic systems which modulate corticotropin-releasing factor release in brain.
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PMID:Acute effects of cocaine on plasma adrenocorticotropic hormone, luteinizing hormone and prolactin levels in cocaine-dependent men. 133 1

Minimally invasive operations such as laparoscopic cholecystectomy appear to result in more rapid recovery of normal function, less physiological disturbance, and presumably less stress to the organism than open operation counterparts. The purpose of this study was to determine the stress response associated with minimally invasive surgery compared to conventional laparotomy. Three groups of pigs underwent general endotracheal anesthesia. The first group had laparoscopic cholecystectomy, the second open cholecystectomy, and the last group (controls) had only general anesthesia. The neuroendocrine serum stress markers adrenocorticotropic hormone (ACTH), cortisol, insulin, and glucagon were measured prior to anesthesia and for the first 3 postoperative days. Analysis of the data showed significant elevations of both ACTH and cortisol for laparoscopic operations as well as for open operation (cortisol only) in the immediate postoperative period. No differences were found for the other serum stress markers. We conclude that minimally invasive surgery in this porcine model confers no advantage, as measured by four neuroendocrine stress hormones, over conventional surgery. Further study is required to determine the clinical implication of these findings.
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PMID:Neuroendocrine stress response after minimally invasive surgery in pigs. 133 96

Patients with systemic lupus erythematosus (SLE), systemic scleroderma (SSD) and donors were examined for the blood levels of adrenocorticotropic hormone, hydrocortisone, follicle-stimulating hormone, luteinizing hormone, prolactin, estradiol, testosterone, progesterone, thyroid-stimulating hormone, triiodothyronine, thyroxin, and insulin. The corticotropin load test was carried out in 38 SLE patients, 32 SSD patients and 24 donors. The prednisolone test was made in 15 SSD patients and 27 donors. The studies were made with the aid of RIA. The patients with SLE manifested a decline of the basal level of hydrocortisone as well as a reduction of the reserve potentialities of the pituitary-adrenal system. The patients with SSD demonstrated a negligible decrease of the basal level of hydrocortisone with an evident lowering of the reserves of the same system. The treatment of SLE and SSD patients with glucocorticoids was followed by marked hyperinsulinemia.
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PMID:[An analysis of the hormonal response during the performance of stress tests in patients with systemic lupus erythematosus and systemic scleroderma]. 133 48

Endocrine responses to the serotonin (5-HT) 5-HT1C/5-HT2 agonist (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) were utilised to evaluate cocaine-induced alterations in postsynaptic 5-HT receptor function. Rats received cocaine HCl (0, 5 or 15 mg/kg i.p.) twice daily for 7 days. Effects of DOI (0, 0.5, 2 or 10 mg/kg i.p.) on plasma adrenocorticotropic hormone (ACTH), corticosterone, prolactin, oxytocin and renin concentrations were assessed 42 h after the final cocaine injection. DOI dose dependently increased the plasma concentrations of each hormone. Cocaine potentiated the DOI-induced elevations of plasma ACTH, corticosterone and prolactin concentrations. In contrast, the oxytocin response was reduced, and the renin response was unaltered by cocaine exposure. The data suggest that 5-HT2 receptor-mediated responses for ACTH, corticosterone and prolactin secretion become supersensitive following repeated cocaine. In contrast, the 5-HT2 receptor-mediated response for oxytocin secretion is subsensitive. The cocaine-induced changes in postsynaptic 5-HT receptor function are likely a consequence of deficits in the function of 5-HT nerve terminals, that we have documented previously.
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PMID:Repeated cocaine modifies the neuroendocrine responses to the 5-HT1C/5-HT2 receptor agonist DOI. 133 68

An altered immunoendocrine feedback regulation within the hypothalamo-pituitary-adrenal axis may modulate the pathogenesis of an avian autoimmune disease. To date studies have been hampered by a lack of reliable, specific, and sensitive methods for determining adrenocorticotropic hormone (ACTH) in chickens. The present study describes the determination of ACTH in plasma of chickens with a commercial radioimmunoassay, the antibody of which binds to the midregion of human ACTH 1-39. The chickens, kept on a 12-hr day and 12-hr night shift with artificial light, showed changes in plasma ACTH concentrations during the light phase with maximum values 8 hr after the light was turned on. ACTH was not measurable after treatment with dexamethasone. Intravenous administration of supernatants from concanavalin A-stimulated spleen cells increased basal plasma ACTH concentrations more than 20-fold within 1 hr. This increase in plasma ACTH was higher and longer lasting in UCD 200 chickens, an animal model for scleroderma, compared with outbred and inbred normal White Leghorn chickens.
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PMID:Investigation of ACTH responses of chickens with autoimmune disease. 133 39


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