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)

Adrenal chromaffin granules contain at least 10 peptides, ranging in size from 3 to 5 kilodaltons, that yield, upon digestion with trypsin, peptides that show specific binding to opiate receptors. All are distinctly different from beta-endorphin. Two of these peptides have been purified to homogeneity and subjected to chemical analysis. One is apparently a [Met]enkephalin precursor containing two copies of the [Met]enkephalin sequence. The other peptide contains both [Leu]enkephalin and [Met]enkephalin sequences and is presumably a common precursor of the two forms of enkephalin.
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PMID:Probable precursors of [Leu]enkephalin and [Met]enkephalin in adrenal medulla: peptides of 3-5 kilodaltons. 624

Two patients developed recurrent Cushing's disease 3 and 7 years after total bilateral adrenalectomy. In the first patient, a 65-year-old man, the adrenal tissue was not localized by radioactive cholesterol scintigraphy. Plain x-ray films of the skull revealed a normal sella turcica. Although clinical improvement resulted from the discontinuation of cortisone replacement therapy, urinary free cortisol levels remained elevated and the patient was treated with pituitary irradiation. Serum and urine cortisol levels gradually returned to normal. Four years after irradiation, the plasma adrenocorticotropic hormone (ACTH) concentration was elevated, but tomography of the sella turcica and urinary cortisol excretion remained normal. The second patient, a 41-year-old man, displayed elevated ACTH levels and x-ray evidence of a pituitary tumor at the time of recurrent Cushing's disease. After trans-sphenoidal hypophysectomy, the hypercortisolism abated and the ACTH concentration returned to normal. Adrenal scintigraphy frequently locates cortisol-secreting tissue in patients with recurrent Cushing's disease, and some investigators suggest treatment by the surgical removal of the adrenal remnant. Although the etiology of Cushing's disease is controversial, current evidence suggests that most cases result from ACTH-producing pituitary tumors. We suggest, therefore, that the anterior pituitary gland may be a more suitable target than the adrenal remnant for the treatment of recurrent Cushing's disease.
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PMID:Recurrent Cushing's disease: successful treatment by pituitary irradiation or trans-sphenoidal hypophysectomy in two cases. 625 6

Adrenal cells were prepared from non-pregnant (anoestrous) sheep, from ewes at days 50, 100 and 130 of pregnancy and at term, and from animals at 1-5 days post partum. The ability of the cells to respond to adrenocorticotrophin (ACTH1-24), alpha-melanocyte-stimulating hormone (alpha-MSH), or combinations of these peptides has been examined in vitro. There was a progressive rise in the basal output of cortisol during pregnancy and in the absence of adrenocorticotrophin the cortisol output from adrenal cells of late pregnant and post-partum sheep the amount of ACTH required to produce half the maximum output of steroid (ED50) was 8 pg/ml. The ED50 increased in early pregnancy to 112 pg/ml and then fell to < 5 pg/ml between day 100 and term. At term both the stimulation ratio and the absolute increment in cortisol output elicited by a maximal concentration of ACTH were greater than at any other time tested in pregnant or non-pregnant sheep. Cortisol output during pregnancy was not increased by alpha-MSH, although at term the stimulatory effect of ACTH1-24 was partially antagonized by alpha-MSH. These results suggest that there may be an increase in the responsiveness of the maternal adrenal during pregnancy, although the factor(s) responsible remains unknown.
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PMID:Increase in the response to adrenocorticotrophin of isolated maternal adrenal cells from sheep in late pregnancy. 625 84

Theophylline is thought to improve asthma by increasing intracellular cyclic adenosine 3'-5'-monophosphate (cAMP) levels. It has been demonstrated in experimental animals that elevation of intracellular cAMP in the adrenal cortex causes an increased secretion of cortisol. We studied whether therapeutic doses of theophylline given intravenously and orally to human subjects over 3 days would increase cortisol secretion. A single-blind, 6-day protocol was employed in five normal and five asthmatic volunteers. Adrenal function was monitored by 8 A.M. and 4 P.M. serum cortisol and adrenocorticotropic hormone (ACTH) levels; daily 24-hr urine for urinary-free cortisol (UFF), 17-hydroxysteroids (17-OH), and 17-ketosteroids (17-KS); and alternate-day cortisol secretory rates (FSR) measured by isotope dilution after intravenous 14C-cortisol. Serum theophylline concentration also was monitored. Results in normal and asthmatic subjects were similar. Theophylline caused a significant but transient increase in UFF and 17-OH excretion. Urine volumes also increased significantly, suggesting that the renal effect of theophylline accounted for the increased UFF and 17-OH excretion. FSR increased during the first 24 hr after theophylline in eight of nine cases (p < 0.05 by sign test), mean values increasing from 14.2 to 19.3 mg, but this effect had dissipated by day 3 of theophylline administration. In contrast to these findings, theophylline had no effect on serum cortisol or ACTH or urinary 17-KS. It is likely that serum cortisol and ACTH remained unchanged because the increase in cortisol secretion was offset by a concomitant increase in cortisol clearance. It is concluded that theophylline produces a small, transient increase in cortisol secretion and clearance, and this effect is similar in asthmatic and normal subjects.
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PMID:Effect of theophylline on cortisol secretion. 625 23

The adrenal gland of the mouse takes up intravenously administered 125I-labeled human low density lipoprotein (LDL) by a high affinity, receptor-mediated mechanism. Uptake is enhanced by treatment of mice with a combination of 4-aminopyrazolopyrimidine, which eliminates endogenous mouse lipoproteins from the plasma, and adrenocorticotropin, which increases the number of adrenal LDL receptors. In the current studies, we show that adrenal uptake of 125I-LDL is blocked when the mice have received a prior intravenous injection of a rabbit antibody directed against the LDL receptor purified from bovine adrenal cortex. The antibody-mediated inhibition of 125I-LDL uptake persisted for 6 h and was reversed by 19 h. Adrenal uptake of 125I-labeled high density lipoprotein was not affected by the antibody, supporting the previous suggestion that high density lipoprotein uptake by the adrenal gland is mediated by a receptor that differs from the LDL receptor. The current studies illustrate the usefulness of antibodies in probing the process of receptor-mediated endocytosis in intact animals.
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PMID:Antibody against low density lipoprotein receptor blocks uptake of low density lipoprotein (but not high density lipoprotein) by the adrenal gland of the mouse in vivo. 626 99

Intracisternal administration of synthetic human beta-endorphin (0.058-7.25 nmol) in chronically cannulated, conscious, freely moving, adult male rats increased plasma concentrations of epinephrine, norepinephrine, and dopamine in a dose-related manner. Epinephrine secretion was the most sensitive to the stimulatory effect of intracerebral beta-endorphin; plasma epinephrine increased transiently in response to 0.058 nmol. Of the three catecholamines, plasma epinephrine showed the greatest and most rapid response to the largest dose (7.25 nmol) studied. Plasma norepinephrine increased significantly in response to 1.45 nmol, peaking later than plasma epinephrine. Plasma dopamine increased only in response to the highest dose examined. These beta-endorphin effects on plasma catecholamines were inhibited by intraarterial naloxone (1.1 mumol/kg), supporting mediation at opioid receptors. Pretreatment with the ganglionic blocking agent chlorisondamine inhibited the responses of all three catecholamines to intracisternal beta-endorphin. Bilateral adrenal denervation completely prevented the plasma epinephrine response to beta-endorphin and blunted the plasma norepinephrine and dopamine responses. Prior intracisternal administration of hemicholinium-3 blocked the plasma responses of all three catecholamines to intracisternal beta-endorphin, providing evidence for the involvement of central cholinergic neurons in the mechanism mediating beta-endorphin-induced increases in plasma catecholamines. The data are consistent with the hypothesis that endorphins act at a presently unknown brain site(s) to increase the central sympathetic outflow to adrenal medulla and peripheral sympathetic nerve endings, thus stimulating peripheral catecholamine release and increasing plasma concentrations of epinephrine, norepinephrine, and dopamine.
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PMID:beta-Endorphin-induced stimulation of central sympathetic outflow: beta-endorphin increases plasma concentrations of epinephrine, norepinephrine, and dopamine in rats. 626 92

Adrenal delta 5-3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) activity was determined in male rate 4, 6, 12, 18 and 24 months of age. Mean (+/- SE) adrenal 3 beta-HSD concentration (microgram delta 4-androstenedione formed/minute/mg tissue), specific activity (microgram/minute/mg protein) and total content (microgram/minute/pair of adrenals) were less (p less than 0.001 to p less than 0.025) in male rats 12 months of age (0.222 +/- 0.010, 1.66 +/- 0.09 and 8.6 +/- 0.8, respectively) or older, than in males four months of age (0.372 +/- 0.011, 2.69 +/- 0.07 and 13.4 +/- 1.1, respectively). Subcutaneous administration of 10 IU adrenocorticotropin daily for a period of five days to male rats 24 months of age elevated adrenal weight by 50 percent and restored dehydrogenase activity to that of the young untreated animal. Therefore, adrenal function in male rats as determined by 3 beta-HSD activity declines with advancing age, but remains responsive to adrenocorticotropic stimulation.
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PMID:Effect of aging and adrenocorticotropin on adrenal delta 5-3 beta-hydroxysteroid dehydrogenase activity in male rats. 626 36

Adrenal function was assessed in dogs after intramuscular administration of a single dose of methylprednisolone acetate (MPA). Twelve dogs were test challenged with adrenocorticotropic hormone (ACTH) and then assigned randomly to 1 of 3 groups and given MPA. Individual groups were test challenged with ACTH 2, 3, or 4 weeks later. All dogs were rechallenged 5 weeks after MPA administration. Plasma cortisol concentration was determined by radioimmunoassay. Basal plasma cortisol (time 0) was depressed on weeks 2 and 3, but not on weeks 4 and 5. Adrenal response to ACTH (increment of cortisol change) was suppressed on weeks 2, 4, and 5, but not on week 3. It was concluded that a single dose of MPA is capable of altering adrenal cortical function in dogs for at least 5 weeks.
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PMID:Adrenocortical suppression in the dog after a single dose of methylprednisolone acetate. 626 93

Hormone production in the human feto-placental unit has been studied extensively yet relatively little is known about the regulatory mechanisms involved. A tissue culture approach has been used to examine the effect of potential controlling factors on steroid production by the human mid-term fetal adrenal and mid-term and term placenta. Adrenal. The pituitary peptides corticotropin (ACTH) and alpha-melanocyte-stimulating hormone (alpha-MSH) had the most significant influence on adrenal steroidogenesis in both the fetal and definitive zones. Their effects were not identical: they enhanced dehydroepiandrosterone sulphate (DHA-S) production in a comparable manner but alpha-MSH had much less of a stimulatory effect on cortisol biosynthesis. Medium from homologous fetal pituitary cultures mimicked the effects of alpha-MSH rather than ACTH. Homologous placental culture medium and progesterone enhanced only cortisol production and only in the fetal zone cells. These results demonstrate that specific fetal pituitary and placental factors influence fetal adrenal activity and suggest a functional zonation of the fetal adrenal. Placenta. DHA, DHA-S and 16-hydroxy-DHA stimulated oestrogen biosynthesis while high concentrations of DHA and DHA-S (but not 16-hydroxy-DHA) inhibited progesterone production. Luteinizing hormone-releasing hormone (LRH) inhibited both oestrogen and progesterone biosynthesis. Placental steroidogenesis can therefore be influenced not only by the fetus, through its increasing adrenal output of oestrogen precursors, but also by factors originating within the placenta itself.
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PMID:Regulation of hormone production in the human feto-placental unit. 627 68

Adrenal cells secrete steroids after stimulation with corticotropin (ACTH), whereas cells reconstructed by fusing adrenal cell nuclei to fibroblast cytoplasms are temporarily (2-3 wk) unresponsive to ACTH. In this report, we characterize this inhibition by using "cybrids" (cytoplasmic hybrids) isolated by either genetic selection or a new procedure that utilizes the fluorescence-activated cell sorter and the vital mitochondrial dye rhodamine 123. Such cybrids, which contain both adrenal and fibroblast cytoplasmic components, are unable to produce steroids, suggesting the existence of cytoplasmic inhibitory factors. In order to elucidate this cytoplasmic inhibition of steroidogenesis, techniques are described that test the contribution of fibroblast mitochondria to this phenomenon. The first technique utilizes purified mitochondria, isolated from chloramphenicol (CAP)-resistant fibroblasts, to confer CAP resistance on an otherwise sensitive adrenal cell. The resulting CAPr cells, termed mitochondrial transformants, are responsive to ACTH. The second technique utilizes a procedure for isolating small fragments of cytoplasm (microcytospheres) from fibroblasts. Microcytospheres, which do not contain mitochondria, are stained with rhodamine 18, a vital membrane dye, and then fused to unstained adrenal cells. The fusion products are then isolated with the fluorescence-activated cell sorter. Approximately 30% of the fusion products are inhibited in their ability to respond to ACTH. These results suggest that the fibroblast cytoplasm contains nonmitochondrial long-lived inhibitory factors that temporarily suppress steroidogenic function in adrenal cells.
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PMID:Long-lived cytoplasmic factors that suppress adrenal steroidogenesis. 628 Jan 68


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