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)

1. Adrenal responses to intra-aortic infusions of pure synthetic ovine corticotrophin-releasing factor (CRF) have been investigated in functionally hypophysectomized calves previously fitted with an adrenal clamp. 2. CRF caused an increase in the output of cortisol from the adrenal gland, which was dose related over the range 4-8 pmol min-1 and maximal at the higher of these doses; this response was observed at a dose below that which produced any change in adrenal vascular resistance. Cortisol output was also found to be related linearly to the rate at which CRF was estimated to be presented to the gland during these infusions. 3. The infusions of CRF also provoked the release of small, but readily detectable, amounts of adrenocorticotrophin-like peptides (ACTH) from the gland. This was mainly in the form of ACTH1-39 with some pro-opiomelanocortin (POMC) also being released. 4. Comparison of the adrenal steroidogenic response to exogenous CRF with that to synthetic ACTH1-24 showed that CRF was the more potent; in each case cortisol output was related linearly to the presentation rate of the peptide. 5. It is concluded that the adrenal cortex in the calf is capable of releasing cortisol in response to exogenous CRF at low concentrations and is even more sensitive to CRF than it is to exogenous ACTH over the dose range that was employed.
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PMID:Adrenal responses to corticotrophin-releasing factor in conscious hypophysectomized calves. 196 66

Among 436 patients with hypertension unrelated to any renal lesion, renovascular damage, pheochromocytoma, Cushing's syndrome or hyperthyroidism, 15 patients had low plasma renin activity (PRA) and elevated plasma aldosterone concentrations in the upright position and resultant high aldosterone/PRA ratios: 8 with aldosterone-producing adenoma (APA; group 1) and 7 with idiopathic hyperaldosteronism (IHA; group 2). Thirty-nine patients had suppressed PRA in the presence of normal plasma aldosterone levels and moderately elevated aldosterone/PRA ratios (group 3). Thirty of them had elevated plasma 11-deoxycorticosterone (DOC) and 18-hydroxy-11-deoxycorticosterone (18-OH-DOC) concentrations (group 3a) and 9 of them had normal levels of those mineralocorticoids (group 3b). The rest of them (382 patients) had low aldosterone/PRA ratios (group 4). Adrenal scintigraphy with dexamethasone pretreatment revealed [13I]-cholesterol accumulation not only in patients with APA (unilateral) or IHA (bilateral), but also in patients of group 3a (bilateral). In patients in groups 3a and 3b adrenal size (especially thickness), as measured by computed tomography (CT scan), was enlarged, as in patients with IHA (group 2), and was significantly greater than in patients of group 4 (p less than 0.001). Spironolactone reduced blood pressure in all tested patients of group 3a, and the removal of adrenal tumor or hyperplastic tissue normalized blood pressure in patients of groups 1, 2 and 3a. Excised adrenal glands exhibited cortical hyperplasia with or without nodular hyperplasia in patients of group 3a. Good agreement was found between the actual size of the excised tissue and the measurement obtained by CT scan. Since beta-endorphin and beta-lipotropin were depressed in patients of group 3a, it is suggested that an unknown pituitary substance stimulates the adrenal cortex to release too large amounts of DOC and 18-OH-DOC and inappropriate secretion of aldosterone.
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PMID:Inappropriate elevation of the aldosterone/plasma renin activity ratio in hypertensive patients with increases of 11-deoxycorticosterone and 18-hydroxy-11-deoxycorticosterone: a subtype of essential hypertension? 207 Mar 75

We compared gastric myoelectrical activity and endogenous neuroendocrine responses in subjects with and without motion sickness elicited by illusory self-motion or vection. Rotating a drum with black and white vertical stripes around seated stationary subjects (n = 22) produced vection. Gastric myoelectrical activity was recorded with cutaneous electrodes. Thirteen subjects developed gastric dysrhythmias [4- to 9-cycles/min (cpm) signals] and motion sickness during vection, whereas nine subjects maintained normal 3-cpm gastric rhythms and remained symptom free. Base-line plasma cortisol and beta-endorphin levels were significantly greater (P less than 0.01) in the subjects who would develop gastric dysrhythmias and nausea compared with the subjects who would not develop motion sickness. Norepinephrine levels increased in the nauseated group immediately after vection ceased (354.6 +/- 41.1 pg/ml) compared with the symptom-free subjects (223.1 +/- 22.8 pg/ml, P less than 0.05). Epinephrine increased significantly (P less than 0.05) after vection only in the nauseated subjects, whereas dopamine levels were not altered by vection in either group. We conclude that 1) anticipatory increases in plasma cortisol and beta-endorphin occurred in subjects who would develop nausea and gastric tachyarrhythmias during vection; 2) endogenous epinephrine and norepinephrine were increased in subjects who had vection-induced nausea and gastric dysrhythmias; and 3) vection stimulates brain-gut interactions, resulting in gastric tachyarrhythmias and complex neuroendocrine responses in subjects with motion sickness.
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PMID:Neuroendocrine and gastric myoelectrical responses to illusory self-motion in humans. 213 78

Prolactin (PRL) responds to several stimuli that elicit release of adrenocorticotropin (ACTH), but does not increase in response to hemorrhage in fetal animals. To determine whether PRL increases after hemorrhage in older animals, 11 immature female swine were prepared chronically under halothane and conditioned behaviorally to lie in a sling. They were bled 14 ml/kg over 5 min. PRL, ACTH, cortisol (F), lysine vasopressin (LVP), and pressure renin activity (PRA) were measured by radioimmunoassay. Epinephrine (EPI) and norepinephrine (NE) were separated by high-performance liquid chromatography. Arterial PRL increased at 0.75 and 1 h (P less than 0.01) and paralleled ACTH and F that peaked at 0.75 h (P less than 0.05 and P less than 0.01, respectively). All three hormones recovered significantly by 4 h. In contrast, PRA and LVP peaked transiently at 0.25 h after hemorrhage and recovered by 1.5 h (P less than 0.05, in each case). EPI and NE did not change significantly. In individual pigs, ACTH and F each showed correlations (Spearman) with PRL that were positive in 10 pigs and significant in six and five pigs, respectively. The pig with the smallest ACTH change (8.4 pg/ml peak) showed no increase in PRL. Peaks in PRL were simultaneous with (five pigs) or delayed by 15 min (four pigs) or 30 min (one pig) from peaks in ACTH. Significant correlations of PRL with PRA and with LVP occurred in only two pigs and in one pig, respectively. A common pathway may contribute to other independent mechanisms controlling the release of ACTH and PRL after hemorrhage.
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PMID:Response of prolactin to hemorrhage is similar to that of adrenocorticotropin in swine. 215 59

Experiments characterized the dynamics of the pituitary and adrenocortical response to noise in awake dogs to determine if a dissociation exists between changes in plasma bioactive (bio) adrenocorticotropic hormone (ACTH) and immunoreactive (ir) ACTH. In addition, experiments determined the temporal relationship between cardiovascular, adrenomedullary, and adrenocortical responses induced by the acute presentation of noise. Trained dogs were prepared chronically with adrenal venous and femoral arterial cannulas. Experiments were done 48-96 h postsurgery and consisted of presentation of noise (75 dB; 0.25-8 kHz) for 3 min (n = 6) or of blood sampling alone (n = 5). In response to noise, mean arterial pressure and heart rate increased at 30 s and returned to base line at 4 min. Adrenal secretion of epinephrine and norepinephrine increased at 1 min and remained elevated until 4 min. Adrenal blood flow increased from 2 to 4 min as the result of a parallel increase in adrenal vascular conductance. Plasma bioACTH increased from 6 to 15 min in parallel with that of plasma irACTH. Before noise, the ratio of bioACTH to irACTH was 0.2-0.3, but the absolute change in bioACTH and irACTH after noise was not different. The increase in plasma ACTH occurred concomitant with or preceded an increase in cortisol secretion. Blood sampling alone caused no change in any variable. These data show that unexpected noise evokes a sequence of responses with rapid onset that includes tachycardia, hypertension, and increases in adrenomedullary secretion and adrenal vascular conductance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pituitary-adrenal and adrenomedullary responses to noise in awake dogs. 215 60

Previous studies indicated that acute exposure of adrenal cells to adrenocorticotropic hormone (ACTH) markedly stimulates steroidogenic capacity in vitro but also inhibits cell proliferation. However, in vivo, ACTH is known to stimulate adrenal cell growth. To address this discrepancy, we determined the effect of long-term (9-11 days) continuous or intermittent exposure to ACTH on human fetal adrenal cell proliferation and steroidogenesis. Adrenal glands from fetuses 18-22 wk gestation were studied. Fetal zone cells were plated either on plastic or on an extracellular matrix (ECM) in the presence and absence of basic fibroblast growth factor (bFGF) (0.5 ng/ml) and 1 or 10 nM ACTH. As determined by cell counting, bFGF stimulated cell proliferation during 9 days in culture. In the presence of bFGF, the average doubling time decreased from 44 to 30 h on plastic and from 37 to 26 h on ECM. Under these conditions, ACTH did not inhibit cell proliferation. Proliferation of fetal adrenal corticosteroid-producing cells in the ACTH-treated cultures also was assessed by histochemical staining for 3 beta-hydroxysteroid dehydrogenase (3 beta HSD). The number of positive cells increased more than 4-fold between Days 5 and 9 in culture. Continuous treatment with 1 nM ACTH increased dehydroepiandrosterone sulfate (DHAS) production 5- to 10-fold during the first 5 days in culture. Thereafter, the stimulated hormone production decreased over time, although there was still a difference of almost 100-fold between the control and ACTH-treated cultures at the end of 9 days.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Maintenance of cell proliferation and steroidogenesis in cultured human fetal adrenal cells chronically exposed to adrenocorticotropic hormone: rationalization of in vitro and in vivo findings. 216 Dec 62

A study was conducted to determine whether within-breed differences in adrenocortical response to exogenous adrenocorticotropin (ACTH) might be accounted for by differences in responsiveness of the adrenocortical cells per se. Large White x Landrace male pigs (n = 20) were used; 10 had high adrenocortical response to ACTH administration and 10 had low response. Five high and 5 low responders were euthanatized at 15 weeks of age, and the remaining 5 high and 5 low responders were euthanatized at 21 weeks of age. Adrenal glands were removed and weighed, and adrenocortical cells were dispersed by tryptic digestion and incubated for 2 hours with synthetic ACTH at concentrations ranging from 0.5 to 10,000 pg/ml. Samples were taken at 30-minutes intervals, and cortisol concentration was determined by use of a radioimmunoassay. Results indicate that for pigs of both age groups, high responders had heavier adrenal glands, with higher adrenocortical cell density and higher cell yield than did low responders. Synthetic ACTH had a stimulatory effect on dispersed porcine adrenocortical cells, as indicated by changes in cortisol concentration in vitro. Adrenocortical cells from high responders produced less cortisol, on a per-cell basis, than did those from low responders. However, when corrected for total cell yield, the potential cortisol production by each pair of adrenal glands was significantly (P less than 0.05) higher in the high responders than in the low responders. Thus, high-responding pigs have larger adrenal glands and higher adrenocortical cell density, which may result in higher output of cortisol after ACTH administration or exposure to stressors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:In vitro study of the function of adrenocortical cells from pigs of differing in vivo response to adrenocorticotropin. 216 17

The insulin-like growth factors (IGFs) may be important autocrine and paracrine mediators of organ growth. We used solution-hybridization/ribonuclease protection assays to examine IGF-I and IGF-II mRNA abundance during hypertrophy or the rat adrenal gland induced by unilateral adrenalectomy or by adrenocorticotropic hormone (ACTH) infusion. Adrenal IGF-I mRNA did not change during the period of rapid organ growth at 18 or 66 h after unilateral adrenalectomy. ACTH infusion induced a time- and dose-dependent decrease in adrenal IGF-I mRNA despite significant increases in gland size. IGF-II mRNA also remained unchanged after unilateral adrenalectomy and decreased after ACTH infusion, to a greater extent than IGF-I mRNA. Liver IGF-I mRNA did not change with ACTH exposure, indicating an effect specific to the adrenal. We also measured adrenal P450scc mRNA as a marker of steroidogenic capacity. P450scc mRNA was unchanged after unilateral adrenalectomy and increased with ACTH infusion. Thus IGF-I and IGF-II mRNAs respond in parallel, but in different fashions with different stimuli for adrenal growth. The decrease in IGF mRNA after exposure to ACTH may be a factor in the ACTH-induced inhibition of compensatory hypertrophy after unilateral adrenalectomy.
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PMID:Rat insulin-like growth factor-I and -II mRNAs are unchanged during compensatory adrenal growth but decrease during ACTH-induced adrenal growth. 226 16

1. The effects of 72 h subcutaneous infusion of graded doses of rat CRF and ACTH(1-24) were studied in rats of initial weight 150-170 g. Rat CRF was infused at 30, 100 or 300 ng/h, and ACTH(1-24) at 125, 250 or 500 ng/h. 2. There was a progressive though modest increase in adrenal weight for all CRF doses, and an associated reduction of thymus weight. Circulating ir-ACTH, ir-beta-endorphin and corticosterone levels, and adrenal DNA content, were not increased after 3 days. Adrenal RNA and protein content were increased at the highest CRF dose used. 3. ACTH infusion caused a progressive increase in adrenal weight and thymic involution which was marked at the higher doses; circulating corticosterone levels were not significantly altered by the lowest dose but were significantly raised by the higher doses. As expected, plasma ir-beta-endorphin was suppressed to low levels with all doses. Adrenal DNA did not alter but there were progressive increases in adrenal protein and RNA. 4. There was a marked difference in gain between the two infusion regimens in terms of all parameters measured, suggesting that potent mechanisms exist to temper the pituitary-adrenal response to markedly different levels of peripheral CRF input. The damped effect of CRF infusion compared with that of ACTH may represent desensitization of CRF receptors at the pituitary; alternatively, it may reflect binding and substantial inactivation of CRF in peripheral blood.
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PMID:Effect of 3 day infusion of ACTH or CRF on the pituitary-adrenal axis. 248 98

Cell surface ligand-receptor interactions play a central role in the regulation and expression of macrophage function. Included among these macrophage membrane receptors are the beta-adrenergic and opioid receptors. We studied the abilities of epinephrine, met-enkephalin, forskolin, and adenosine 3':5' cyclic monophosphate (cAMP) analogues to affect macrophage morphology, spreading, and adherence. Cell spreading was quantitated by measuring the perimeters of adherent cell images recorded by videomicroscopy. Epinephrine induced a dose-dependent decrease in macrophage spreading; at 10(-5) M epinephrine the mean perimeter was 10.4 +/- 0.3 microns in comparison to 15.0 +/- 1.0 microns for controls. The inhibition of spreading can be blocked by the antagonist propranolol. On the other hand, met-enkephalin induced a dose-dependent increase in macrophage spreading, with a perimeter of 18.5 +/- 1.0 microns at 10(-8) M. Since catecholamines and opioids are simultaneously released from chromaffin cells of the adrenal, we examined the combinative effects due to treatment with both ligands. When macrophages were exposed to 10(-5) M epinephrine and 10(-8) M met-enkephalin, cell morphology and spreading were indistinguishable from that due to 10(-5) M epinephrine alone. The epinephrine dose-response curve in the presence of 10(-8) M met-enkephalin was similar to that of epinephrine alone. The beta-adrenergic receptor is apparently capable of diminishing or abrogating the opioid receptor signal(s). These combinative and epinephrine-mediated effects may be at least partially accounted for by the action of cAMP. Forskolin and the cAMP analogues N6-2'-O-dibutyryladenosine 3':5' cyclic monophosphate (dbcAMP) and 8-bromoadenosine 3':5' cyclic monophosphate (Br-cAMP) affected cell morphology and spreading in the same fashion as epinephrine. These differences in morphology and spreading behavior were accompanied by changes in the distribution of F-actin, as judged by phalladicin staining and fluorescence microscopy. We suggest that cAMP and microfilaments play important roles in receptor-mediated neuroregulation of macrophage function.
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PMID:Combinative ligand-receptor interactions: effects of cAMP, epinephrine, and met-enkephalin on RAW264 macrophage morphology, spreading, adherence, and microfilaments. 253 24


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