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)

In rats hyperprolactinemia increases corticotropin-releasing hormone (CRH) concentration and secretion in hypophysial portal blood and the serum concentration of adrenocorticotropic hormone (ACTH). To determine whether the stimulatory effect of prolactin (PRL) on CRH and ACTH in vivo is exerted directly on the hypothalamus, hypothalamic explants and primary anterior pituitary cell cultures from adult male and female rats were used. Hypothalami explanted from male and female rats were preincubated during 90 min and treated for 30 min with rat PRL (rPRL) at concentrations of 10(-8), 10(-7), and 10(-6) M (about 200, 2,000, and 20,000 ng/ml, respectively), corticosterone at concentrations of 10(-7), 10(-6), and 10(-5) M (about 35,350 and 3,500 ng/ml, respectively), ACTH at concentrations ranging from 10(-10) to 10(-7) M (0.46, 4.6, 46, and 460 ng/ml, respectively), and graded concentrations of testosterone or estradiol. Concentrations of immunoreactive CRH (iCRH) were measured by radioimmunoassay. rPRL at 10(-6) M stimulated iCRH secretion by 360 and 400% of the basal iCRH output (about 14 pg/hypothalamus), respectively, from hypothalami explanted from male and female rats. ACTH and corticosterone did not suppress rPRL (10(-6) M) induced iCRH secretion. Corticosterone at the concentration of 10(-6) M potentiated rPRL (10(-6) M) induced iCRH secretion in hypothalami explanted from male, but not female rats. Gonadal steroids had no effect either on the basal or rPRL (10(-6) M) stimulated iCRH secretion, with the exception of estradiol which augmented the response to 10(-6) M rPRL by about fivefold, but only at the concentration of 10(-8) M (about 2.7 ng/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prolactin stimulates rat hypothalamic corticotropin-releasing hormone and pituitary adrenocorticotropin secretion in vitro. 165 72

A number of changes in anterior pituitary corticotrophs occur after chronic footshock. These include increased ACTH and beta-endorphin content and a loss of glucocorticoid negative feedback on corticotropin-releasing hormone (CRH)-stimulated ACTH and beta-endorphin secretion, without changes in sensitivity to ovine CRH examined in vitro. The present studies were undertaken to determine whether the in vitro changes were reflected by similar changes in vivo. We developed a fast feedback paradigm using a 5-min swim stress as challenge, with injection of saline or corticosterone immediately prior to swim. Corticosterone reliably decreased ACTH and beta-endorphin responses to swim over the 30-min period studied. This feedback inhibition did not occur in rats that were either exposed to 30 min of chronic footshock for 7 or 14 days or in rats that were treated with corticosterone daily for 14 days in a regimen that has been reported to decrease hippocampal glucocorticoid receptors. By contrast, in rats exposed to the less intense stimulus of 30 min swim for 14 days, the fast feedback action of corticosterone was intact. These results suggest that both fast and delayed feedback corticosterone-inhibitory mechanisms may be blocked by relatively high levels of chronic stress or by chronic treatment with corticosterone, possibly as a consequence of decreased hippocampal glucocorticoid receptor number.
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PMID:Decreased sensitivity to glucocorticoid fast feedback in chronically stressed rats. 216 11

To examine whether an acute pituitary-adrenal response to stress may occur in vivo in the absence of hypothalamic-pituitary connections, we measured plasma beta-endorphin (beta-EP) and corticosterone (C) in rats after acute thermal injury. beta-EP rose significantly after thermal injury in normal rats and rats bearing pituitary-to-kidney autotransplants but not in animals with pituitary aspiration without reimplantation. Corticosterone responses paralleled beta-EP but were significant only in normal controls. Propranolol pretreatment did not reduce postburn beta-EP and C rises in autotransplanted animals. Therefore, since circulating factors contribute in vivo to pituitary-adrenal responses, the widespread practice of using "stress hormone" responses to quantitate perioperative stress or pain may in some circumstances be flawed.
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PMID:Pituitary-adrenal stress response in the absence of brain-pituitary connections. 252 79

Hemidecortication (HD) (left cerebral hemisphere) was performed in rats with the aim of analyzing the modulating effect of the cerebral cortex on the hypothalamic-pituitary-adrenal axis. Corticosterone release induced either by ether or immobilization stress was evaluated in control (C) and HD rats. The percentage increase in corticosterone was greater in HD than in C rats after 15 min of ether stress (HD = 142%, C = 50%) and after 60 min of immobilization stress (HD = 197%, C = 126%). An in vitro test showed that the release of ACTH induced by corticotropin releasing hormone (CRH) from hemipituitary fragments from HD rats was not different from that in control rats. These results suggest an inhibitory effect of the cerebral cortex on the hypothalamus which may modulate the secretion of corticotropin releasing peptides.
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PMID:Ether and immobilization stress effects on pituitary adrenal function in hemidecorticate rats. 262 Jan 93

The effects of previous chronic administration of the tricyclic antidepressant drug chlorimipramine (CMI) on some physiological responses of adult male rats to stress has been studied. CMI significantly reduced food intake and body weight gain, but did not alter either adrenal weight or basal serum corticosterone levels. Corticosterone response to 1 h of immobilization stress was the same in saline and CMI-treated rats. When the rats previously treated with CMI were subjected to chronic immobilization stress, it was found that the drug did not alter the anorexic effects of the stressor, but reduced the rate of adaptation of adrenocorticotropin response to stress. These data indicate that previous chronic CMI administration does not prevent changes in the secretory activity of the pituitary-adrenal system or the reduction of food intake and body weight caused by strong stressors.
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PMID:Previous chronic chlorimipramine treatment did not modify some physiological responses to acute and chronic stress in rats. 283 68

To investigate the involvement of different brain sites in the mediation of glucocorticoid feedback action, we implanted dexamethasone or corticosterone containing glass capillaries into the paraventricular and arcuate nuclei of the hypothalamus, into the lateral septum, the dorsal and ventral hippocampus, amygdala and the cerebral cortex of adrenalectomized male rats, and compared the plasma adrenocorticotropin (ACTH) values to those of the sham implanted controls. The ACTH hypersecretion of adrenalectomized (ADX), sham implanted rats (670 fmol/ml) was reduced significantly by dexamethasone implants placed into the paraventricular nucleus (9.97 fmol/ml), arcuate nucleus (20.54 fmol/ml) or lateral septum (44.15 fmol/ml). Corticosterone was effective only when placed into the dorsal hippocampus, but normal ACTH levels were not restored (219.67 fmol/ml). All other implants at other sites had no effect on ACTH secretion. Our results suggest that corticosterone and dexamethasone possess different feedback potencies and act at different sites in the brain to normalize the ADX-induced ACTH secretion.
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PMID:Corticosterone and dexamethasone act at different brain sites to inhibit adrenalectomy-induced adrenocorticotropin hypersecretion. 285 89

Animals with the viable yellow (Avy/a) gene and their corresponding lean control black mice (a/a) were adrenalectomized or sham adrenalectomized, and changes in body weight, body composition, corticosterone, and GDP-binding to mitochondria isolated from interscapular brown adipose tissue (IBAT) were measured. Adrenalectomy slowed the weight gain of both the yellow obese mice and the black lean mice, but the reduction was greater in the yellow mice. Food intake was significantly reduced in the yellow mice. Adrenalectomy in the yellow mouse was associated with an increase in lean mass and a significant decrease in weights of fat depots. Blood glucose concentrations of the adrenalectomized yellow mice were reduced to levels similar to those of lean mice, but insulin levels, although lower than sham-adrenalectomized yellow mice, remained significantly higher than in lean animals. GDP binding to IBAT mitochondria increased after adrenalectomy in both phenotypes to values that were similar. Corticosterone replacement in adrenalectomized yellow mice produced a dose-dependent increase in body weight that was associated with a decrease in muscle weight and an increase in adipose tissue weight. Both desacetyl-melanocyte-stimulating hormone (MSH) and alpha-MSH interacted with corticosterone to increase body weight gain of adrenalectomized yellow mice. Desacetyl-MSH was more effective than alpha-MSH on increasing adipose tissue and liver weights. The effects of desacetyl-MSH on food intake, weight gain, and tissue weights were independent of the adrenal gland or of corticosterone.
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PMID:Adrenalectomy and response to corticosterone and MSH in the genetically obese yellow mouse. 291 1

Metabolic defects in obese (fa/fa) Zucker rats have previously been shown to be reversed by adrenalectomy; however, hypercorticosteronemia has not been demonstrated. We now report that the total daily excretion of corticosterone and urea nitrogen are significantly greater (P less than 0.01) in obese Zucker rats than in age-matched lean Zucker rats. This excessive excretion of corticosterone is not of autonomous adrenal origin, since dexamethasone treatment (20 micrograms/kg X day) for 2 days induced a proportionate reduction in corticosterone excretion (approximately 50%) in both obese and lean Zucker rats. Corticosterone excretion was further suppressed to levels not different from those in lean rats after 2 days of dexamethasone (40 micrograms/kg X day). Both the peak and total pituitary beta-endorphin secretion in response to an iv bolus of corticotropin-releasing factor (CRF) were diminished in obese Zuckers. The response to CRF in obese Zucker rats was dampened and superimposable on that of dexamethasone-treated lean Zucker rats, suggesting the existence of chronic hypercorticosteronemia as a component of this genetic obesity. These observations provide evidence for a compensatory alteration of the pituitary-adrenal axis. We suggest that corticosterone turnover may be increased in obese Zucker rats.
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PMID:Hypercorticosteronuria and diminished pituitary responsiveness to corticotropin-releasing factor in obese Zucker rats. 293 45

The antinociceptive effect of parenterally and intracerebroventricularly injected morphine and beta-endorphin in adrenalectomized rats and in adrenalectomized rats treated with adrenal steroids was examined employing the hot-plate method. (1) Adrenalectomy sensitized the rats to an analgesic effect of morphine and beta-endorphin. (2) Replacement therapy (chronic and acute) with corticosterone, dexamethasone or RU 28362 (glucocorticoid receptor agonist) effectively reversed the increase in the sensitivity to the analgesic effect of peripherally injected morphine (5 mg/kg i.p.) induced by adrenalectomy to the level of sham-operated animals. Glucocorticosteroids administered to non-adrenalectomized rats did not change the sensitivity to morphine. (3) Corticosterone had a biphasic, dose-dependent effect; the most significant attenuation of the hypersensitivity to morphine-induced antinociception in adrenalectomized rats was achieved after 0.01 mg and after 10 mg (per kg b.w.). Doses of corticosterone of 0.005 mg/kg and in a range of 0.05-0.30 mg/kg were ineffective. (4) Corticosterone in a dose of 0.01 mg/kg (s.c.) had suppressant effects on the adrenalectomy-induced increase in the sensitivity to antinociception induced by morphine when given prior to morphine (60, 30 and 5 min) as well as after the injection of morphine (before the first and the second testing on the hot-plate, 15 and 5 min, respectively). (5) Intracerebroventricularly (i.c.v.) injected morphine and beta-endorphin also displayed the hypersensitivity to the analgesic effect in adrenalectomized rats which in both cases could be suppressed by 0.01 mg/kg of corticosterone given subcutaneously 5 min prior to administration of the opiate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Corticosteroid effects on morphine-induced antinociception as a function of two types of corticosteroid receptors in brain. 296 13

We tested the hypothesis that the increase in adrenocortical system activity is controlled by an error signal generated by the difference between a central reference, or set point, value and some aspect of circulating corticosterone levels in rats maintained on a 12-h light, 12-h dark cycle. The test rats were treated with cyanoketone, an inhibitor that blocks conversion of pregnenolone to progesterone; control rats were treated with vehicle. Test and control rats were fitted with arterial cannulas and, after recovery, continuously collected blood was sampled for plasma corticosterone at 5-min intervals over 2-h periods at five times during the day. Samples were collected at the end of each period for plasma adrenocorticotropin (ACTH). Corticosterone and ACTH levels were similar in the two groups of rats at the nadir (0-2 h after lights-on) and at the peak (0-2 h after lights-off) of the diurnal rhythm. During the time of the maximal diurnal rise in corticosterone (8-10 and 10-12 h after lights-on), test rats had lower mean corticosterone and higher ACTH levels than controls. Infusion of 8 micrograms corticosterone during the 2 h before lights-out did not significantly elevate mean corticosterone levels but decreased end ACTH levels in test rats, whereas similar infusions in control rats resulted in decreased mean corticosterone levels and no change in end ACTH. We conclude that the nyctohemeral rise in ACTH is driven by an error signal resulting from the difference between a central set point value and some aspect of plasma corticosterone levels.
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PMID:Closed-loop feedback control of the nyctohemeral rise in adrenocortical system function. 298 39


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