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)

ACTH was measured with both C-terminal and midportion antibodies in monkey hypophyseal portal plasma, and compared to levels in monkey peripheral plasma, medial basal hypothalamus, and anterior pituitary. In nine female monkeys, mean hypophyseal portal blood C-terminal ACTH immunoactivity was 5290 +/- 2010 (SEM) pg/ml, whereas the mean midportion ACTH level was 949 +/- 178 pg/ml. These immunoactivities were not lower in two monkeys that were completely hypophysectomized 30 min before portal blood collection. The ratio of C-terminal to midportion ACTH immunoactivity was 4:1 in two monkey medial basal hypothalami, and 1:1 in four monkey anterior pituitary glands. Gel filtration of hypophyseal portal plasma extract and of medial basal hypothalamus showed that the C-terminal ACTH immunoactivity eluted in the same position as the corticotropin-like-intermediate lobe peptide standard. The similarity of the C-terminal to midportion ACTH ratios in monkey medial basal hypothalamus and portal blood, and the observation that ACTH immunoactivity was not significantly lower in two hypophysectomized monkeys suggests that portal blood C-terminal ACTH immunoactivity is of hypothalamic rather than pituitary origin. We conclude that monkey hypophyseal portal blood contains high levels of a C-terminal fragment of ACTH, which coelutes with corticotropin-like intermediate lobe peptide on gel filtration, and which is secreted from the brain directly into the portal circulation.
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PMID:Adrenocorticotropin immunoactivity in monkey hypophyseal portal blood. 632 53

A Mr 26,000 corticotropin (ACTH)-like material is present in glacial acetic acid extracts of all normal rat extrapituitary tissues. In the present study, beta-melanotropin (beta-MSH) immunoactivity was detected in glacial acetic acid extracts of normal rat extrapituitary tissues. beta-MSH immunoactivity was also present in all extracts (mean +/- SEM, fmol/mg of protein): brain, 71.0 +/- 16.3; stomach, 11.5 +/- 1.6; kidney, 8.9 +/- 0.8; colon, 8.2 +/- 1.1; small intestine, 6.5 +/- 1.1; liver, 4.3 +/- 0.5; and heart, 3.2 +/- 0.5. Except in brain extracts, beta-MSH and ACTH immunoactivities of tissue extracts were strongly correlated to each other (r = 0.79; n = 42). When tissue extracts (except brain) were passed through a Sephadex G-75 (superfine) column, ACTH and beta-MSH immunoactivities were eluted in a single peak corresponding to Mr 26,000. In contrast, for brain extracts, the MrS of major peaks of ACTH and beta-MSH immunoactivities were 4,500 and 8,000, respectively; a smaller peak of Mr 26,000 ACTH/beta-MSH-like material was also eluted. Specific anti-ACTH immunocolumns, which did not bind purified synthetic beta-MSH, adsorbed both ACTH and beta-MSH immunoactivities of all tissue extracts except those of brain. One-third of the beta-MSH immunoactivity in brain extracts adsorbed to the anti-ACTH immunocolumn, but two-thirds of beta-MSH immunoactivity passed through the column. We conclude that ACTH and beta-MSH immunoactivities are present in all normal rat extrapituitary tissues and exist in most tissues on the same molecule. This Mr 26,000 molecule is closely related to the pituitary ACTH/beta-lipotropin common precursor.
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PMID:Corticotropin/lipotropin common precursor-like material in normal rat extrapituitary tissues. 657 17

Forms of congenital adrenal hyperplasia resulting from deficient steroid hydroxylation at positions 21, 17 alpha, and 11 beta have several similar clinical and biochemical characteristics. Biochemical diagnosis has been dependent on the demonstration of elevated plasma or urinary concentrations of metabolites of the immediate biosynthetic precursor before the enzymatic block, especially after stimulation with adrenocorticotropin. Aldosterone, 18-hydroxycorticosterone, and 18-hydroxydeoxycorticosterone are not closely involved nor are they immediate precursors of any of these enzymatic defects. However, simultaneous determination of the baseline plasma levels of these steroids in patients with nonsodium-losing 21-hydroxylase deficiency (n = 12), 17 alpha-hydroxylase deficiency (n = 6), and 11 beta-hydroxylase deficiency (n = 2) revealed a consistent and distinct pattern (mean +/- SEM in nanograms per deciliter): aldosterone (28.1 +/- 2.8) and 18-hydroxycorticosterone (84.5 +/- 9.2) levels were elevated and 18-hydroxydeoxycorticosterone (8.0 +/- 0.8) levels were within normal limits in 21-hydroxylase deficiency; 18-hydroxycorticosterone (327.2 +/- 73.9) and 18-hydroxydeoxycorticosterone (236.0 +/- 33.8) levels were elevated and aldosterone (3.5 +/- 0.6) levels were reduced in 17 alpha-hydroxylase deficiency; levels of all three steroids (aldosterone 2.6 +/- 0.4, 18-hydroxycorticosterone 5.1 +/- 3.1, 18-hydroxydeoxycorticosterone 0.9 +/- 0.1) were reduced in 11 beta-hydroxylase deficiency. It is suggested that simultaneous measurement of these three steroids can be useful in identifying and further characterizing each of these forms of congenital adrenal hyperplasia.
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PMID:Distinctive plasma aldosterone, 18-hydroxycorticosterone, and 18-hydroxydeoxycorticosterone profile in the 21-, 17 alpha-, and 11 beta-hydroxylase deficiency types of congenital adrenal hyperplasia. 660 48

An enhanced hypothalamo-pituitary-adrenocortical (HPA) activity has been described during onset of elevated blood pressure in spontaneously hypertensive rats (SHR). An instability of the HPA axis could thus contribute to the development of hypertension in these animals. Glucocorticoid effects on blood pressure and HPA function were studied therefore in SHR and normotensive Wistar-Kyoto (WKY) and Wistar rats. Beginning at 4 weeks of age, the rats were treated with 0.1 and 0.5 microgram betamethasone per milliliter drinking water for 7 weeks. SHR and WKY responded with a significant elevation in average blood pressure. In SHR, mean blood pressure rose from 181.4 +/- 3.9 (mean +/- SEM) to 203.1 +/- 2.8 mm Hg in response to the lower dose of betamethasone and to 209.2 +/- 4.0 mm Hg in response to 0.5 microgram betamethasone per milliliter drinking water. In WKY, blood pressure increased from 134.4 +/- 3.3 to 148.2 +/- 3.0 and 157.9 +/- 4.5 mm Hg in response to the lower and higher dose of betamethasone, respectively. No significant effect was seen in Wistar rats, where the mean blood pressure values changed insignificantly from 133.8 +/- 2.1 to 136.3 +/- 3.2 and 135.6 +/- 2.4 mm Hg. Stress-induced secretion of corticosterone was significantly suppressed in a dose-dependent manner in all three strains. Stress-induced secretion of adrenocorticotropin was markedly reduced by 0.5 microgram betamethasone per milliliter in SHR and by both doses in WKY. No significant effect, however, was seen in Wistar rats. A predisposition to the hypertensiogenic actions of glucocorticoids was found therefore in SHR and WKY, but not in Wistar rats.
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PMID:Long-term effects of betamethasone on blood pressure and hypothalamo-pituitary-adrenocortical function in spontaneously hypertensive and normotensive rats. 664 25

The action of human growth hormone (hGH) on plasma lipotropins (beta-and gamma-LPH) in 15 GH deficient patients was studied by comparing the effects induced by the acute administration of the extracted and biosynthetic molecules. The purified extracted preparation (6 mg/m2 im) induced a dramatic rise in plasma LPH: basal (49 +/- 12 pg/ml (mean +/- SEM); peak 1,658 +/- 262 pg/ml. The same dose of biosynthetic methionyl-hGH (met-hGH) induced no significant change in plasma LPH. Both preparations caused identical plasma GH increases. Six different commercially available extracted hGH preparations (Choay, France; Serono, Italy; France Hypophyse, France; Kabi, Sweden; Nordisk, Denmark; International Standard, Great Britain) all showed definite cross-reactivity in the LPH radioimmunoasay, varying from 0.1 to 1.0%, on a weight basis. No cross reactivity was found with met-hGH (less than 0.0001%). On gel exclusion chromatography, the LPH immunoreactivity of the purified preparations was dissociated from the GH immunoreactivity and eluted at the position of beta-and gamma-LPH. These data show that extracted hGH preparations are all contaminated with LPH and raise the question of the possible consequences of chronically elevated plasma LPH in treated patients. The use of biosynthetic met-hGH should prevent this occurence.
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PMID:Plasma lipotropin increase in man after growth hormone administration. Comparison between extractive and biosynthetic hormones. 684 66

Enkephalins inhibit guinea pig ileum contractions in vitro; in vivo they increase gastric contraction strength and small intestinal spike activity in dogs and stimulate tonic and phasic contractile activity of the human colon. This study investigated the question as to whether the stimulatory effect of the synthetic met-enkephalin analogue FK 33-824 on the human colon is antagonized by the narcotic antagonist naloxone. On 3 experimental days 12 healthy young males received in random order (a) 4 mg (subjects 1-6) or 10 mg (subjects 7-12) naloxone i.v. followed by 1 mg FK 33-824 i.m., (b) saline i.v. followed by 1 mg FK 33-824 i.m. and (c) saline i.v. followed by saline i.m. FK 33-824 following saline produced a rapid increase of tonic intraluminal pressure (mean increase: 9.9 +/- 2.5 SEM mmHg; P less than 0.001), an increase in contractions from 1.6 +/- 0.4 to 3.3 +/- 0.8 per min (P less than 0.001), a shift in the dominant frequency of rhythmic contractions from 1.0 +/- 2.5 to 2.5-3.5 cycles per min, an increase in the amplitude of contractions from 10.1 +/-0 2.1 to 15.0 +/- 3.2 mmHg (P less than 0.01), and in the sum of the amplitudes as an overall measure of contractile activity from 148.6 +/- 36.7 to 482.9 +/- 136.9 mmHg (P less than 0.01). All effects lasted for more than 70 min; peak changes occurred in the first 15 min and subsided slowly in intensity. The effects of FK 33-284 were greatly attenuated by premedication of 4 mg naloxone, and abolished, at least for 15-30 min, by 10 mg naloxone. Saline caused no changes. It is concluded that the stimulatory effects of FK 33-824 on human colonic motility are antagonized by naloxone.
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PMID:Stimulatory effects of the synthetic enkephalin analogue FK 33-824 on colonic motor activity antagonized by naloxone. 721 44

It is well established that the central alpha 2-adrenergic agonist clonidine can enhance growth hormone (GH) secretion in humans. This effect is most likely due to stimulation of hypothalamic growth hormone releasing hormone (GHRH) release. To determine the potency of the new I1-imidazoline receptor agonist moxonidine to release pituitary hormones, 12 normal volunteers received clonidine (0.3 mg), moxonidine (0.3 mg), or placebo orally according to a randomized, double-blind protocol. Blood was drawn prior and up to 180 min after drug administration for determination of GH, adrenocorticotropic hormone (ACTH), prolactin, thyrotropin (TSH), luteinizing hormone (LH), follicle-stimulating hormone (FSH), glucose, clonidine, and moxonidine concentrations. The results were compared to those obtained in a standard GHRH stimulation test (1 microgram/kg i.v.). Serum GH levels increased significantly in response to GHRH, clonidine, and moxonidine. However, the increase was less pronounced in response to clonidine and moxonidine as compared to GHRH (mean +/- SEM): after clonidine, GH increased from 0.2 +/- 0.1 to 5.4 +/- 1.5 ng/ml, p < 0.05; moxonidine increased GH levels from 0.1 +/- 0.04 to 4.8 +/- 1.9 ng/ml (p < 0.05); GHRH caused an increase from 0.01 +/- 0.05 to 14.8 +/- 2.5 ng/ml (p < 0.05). No significant change was observed in the concentration of any other pituitary hormone. We conclude that the new I1-imidazoline receptor agonist moxonidine stimulates GH release to a similar extent as clonidine.
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PMID:Growth hormone secretion in response to the new centrally acting antihypertensive agent moxonidine in normal human subjects: comparison to clonidine and GHRH. 758 24

Twelve Taiwanese patients with classic congenital adrenal hyperplasia and 86 family members underwent human leukocyte antigen (HLA) genotyping and the 60-minute adrenocorticotropic hormone (ACTH) stimulation test. The baseline serum 17-hydroxyprogesterone level (mean +/- SEM) before ACTH testing was 1.595 +/- 792 nmol/L in homozygotes, 4.6 +/- 0.5 nmol/L in heterozygotes, and 2.1 +/- 0.8 nmol/L in the unaffected group. The stimulated serum 17-hydroxyprogesterone level (mean +/- SEM) was 1.926 +/- 778 nmol/L in homozygotes, 20.6 +/- 0.9 nmol/L in heterozygotes, and 6.8 +/- 0.6 nmol/L in the unaffected group. There was minimal overlap among the heterozygote and unaffected groups. The 60-minute ACTH stimulation test can provide clinicians with hormonal criteria for the assessment of the genotype of classic 21-hydroxylase deficiency in the Chinese population.
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PMID:Genotype of classic congenital adrenal hyperplasia and the 60-minute adrenocorticotropic hormone stimulation test. 761 27

Acute stress results in activation of the hypothalamic-pituitary-adrenal (HPA) axis. ACTH and cortisol secretion is stimulated by corticotropin-releasing hormone (CRH). It has also been shown that activation of the HPA axis during stress is accompanied by changes in the immune response. However, little is known about the influence of acute stress on the release of cytokines such as interleukin-1 (IL-1) or interleukin-2 (IL-2). In this study, we determined serum IL-1 alpha and IL-2 levels in 19 patients undergoing the acute stress of angioplasty for coronary artery disease. A second protocol was devised to determine serum IL-1 alpha and IL-2 concentrations as well as lymphocyte subpopulations in 10 normal volunteers receiving 1 microgram kg-1 human CRH intravenously. Finally, IL-1 alpha concentrations were measured in CRH-incubated mononuclear cell (MNC) and monocyte cultures. In response to the stress of angioplasty, ACTH and cortisol as well as IL-1 alpha and IL-2 concentrations were clearly above baseline levels (IL-1 alpha, mean +/- SEM, baseline: 1.39 +/- 0.34 ng ml-1, after angioplasty: 2.64 +/- 0.73 ng ml-1, P < 0.05; IL-2, baseline: 1.2 +/- 0.13 ng ml-1, after angioplasty: 2.8 +/- 1.14 ng ml, P < 0.05). A similar pattern was obtained in normal subjects in response to CRH (Il-1 alpha, baseline: 0.8 +/- 0.2 ng ml-1, after angioplasty: 3.7 +/- 1.4 ng ml-1, P < 0.05; IL-2, baseline: 1.9 +/- 0.4 ng ml-1, after angioplasty: 5.4 +/- 2.2 ng ml-1, P < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Systemic interleukin-1 alpha and interleukin-2 secretion in response to acute stress and to corticotropin-releasing hormone in humans. 789 16

The role of the opioid receptor-endogenous opioid peptide system in mediating analgesia induced by nitrous oxide has been a controversial subject. Most previous studies provided only indirect evidence either to support or refute the involvement of opioid receptors and/or endogenous opioid peptides. To provide more direct evidence, we measured concentrations of five naturally occurring endogenous opioid peptides in third ventricular cerebrospinal fluid from eight acclimated dogs with chronically implanted ventricular catheters. Paired samples of cerebrospinal fluid were obtained from each animal when breathing room air or 66-75 vol% nitrous oxide in oxygen through a face mask. Endogenous opioid peptides were physically separated using reversed phase high-performance liquid chromatography and quantified using radioimmunoassays. Nitrous oxide inhalation increased cerebrospinal fluid concentrations of met5-enkephalin from a control value of 0.30 +/- 0.07 (mean +/- SEM, n = 8) to 42.4 +/- 8.1 pmol/mL (P = 0.0006). Increases ranged from 28 to more than 400 times the control value. Met5-enkephalin-arg6-phe7 concentrations also increased from 14.5 +/- 2.5 to 57.6 +/- 17.8 pmol/mL (P = 0.018). No significant changes were noted in concentrations of dynorphin A, dynorphin B, or beta-endorphin. These results directly support the hypothesis that nitrous-oxide-induced analgesia involves the proenkephalin-derived family of endogenous opioid peptides.
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PMID:Nitrous oxide selectively releases Met5-enkephalin and Met5-enkephalin-Arg6-Phe7 into canine third ventricular cerebrospinal fluid. 789 15


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