UNIPROT:P01189 - FACTA Search

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Query: UNIPROT:P01189 (beta-endorphin)
21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypotensive functional haemorrhage induced by venous pooling of blood in the legs has been reported to be characterized by a vasovagal reaction. In the present study these observations were extended by determination of the hormonal profile developed during progressive central hypovolaemia and an emotionally induced vasovagal syncope. In six subjects venous pooling resulted in normotensive central hypovolaemia, in one subject hypotensive central hypovolaemia was induced, and one subject experienced an emotionally induced vasovagal syncope. During normotensive central hypovolaemia heart rate increased from 58 +/- 4 to 76 +/- 4 beats min-1 (P less than 0.05) and cardiac output fell from 6.1 +/- 0.4 to 4.1 +/- 0.2 1 min-1. Pulse pressure and central venous pressure decreased from 64 +/- 4 to 53 +/- 4 mmHg, and from 8 +/- 2 to 3 +/- 2 mmHg, respectively. Adrenaline and noradrenaline increased from 87 +/- 10 to 120 +/- 20 pg/ml and from 196 +/- 33 to 370 +/- 50 pg/ml, respectively. Angiotensin II increased from 13 +/- 4 to 36 +/- 6 pg/ml and aldosterone from 63 +/- 9 to 180 +/- 27 pg/ml. In hypotensive central hypovolaemia the decrease in mean arterial pressure was accompanied by a decrease in heart rate and increments in the plasma concentrations of pancreatic polypeptide, indicating increased vagal activity and beta-endorphin, while plasma noradrenaline was unchanged. In emotionally induced syncope heart rate decreased to cardiac arrest for 13 s, associated with increments in the plasma concentrations of pancreatic polypeptide and beta-endorphin. It is concluded that normotensive functional haemorrhage in man is associated with increased sympathetic activity and that the qualitatively similar observations obtained during an emotionally and a hypovolaemic-induced hypotensive episode indicate that the hypotensive functional haemorrhage is characterized by a vasovagal reaction.
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PMID:Progressive central hypovolaemia in man--resulting in a vasovagal syncope? Haemodynamic and endocrine variables during venous tourniquets of the thighs. 360 88

A soluble metalloendopeptidase identified in rat brain, preferentially cleaves bonds in peptides having hydrophobic amino acid residues in the P1, P2, and P3' positions. (The nomenclature of T. Schechter and A. Berger is used to describe the interaction between enzyme and substrate. The amino acid residues in the substrate are designated as P1, P2, P3 etc. in the N-terminal direction and P1', P2', P3' etc. in the C-terminal direction from the bond undergoing cleavage. The corresponding subsites in the enzyme are identified by the letter S.) The degradation of a series of biologically active peptides and their affinity toward the enzyme was studied. Dynorphin-(1-8), alpha-neo-endorphin, and beta-neo-endorphin are rapidly hydrolyzed to form leu-enkephalin, whereas bovine adrenal medulla dodecapeptide is hydrolyzed to form met-enkephalin. The enzyme, however, does not cleave a larger precursor molecule of metenkephalin, such as bovine adrenal medulla docosapeptide. Several other bioactive peptides are also cleaved at sites consistent with our previously reported specificity studies. Met- and leu-enkephalin are resistant to hydrolysis. The binding affinity [as expressed by inhibitory constant (Ki) or Michaelis-Menten constant (Km) values] of several bioactive peptides such as dynorphin-(1-8), beta-neo-endorphin, neurotensin, angiotensin I, and bradykinin was found to be in the micromolar range. These peptides were also rapidly hydrolyzed by the enzyme, showing, as a result, high specificity constants (kcat/Km values). The highest enzyme activity was found in brain, testis, and in the anterior and posterior lobes of the pituitary, while the activity in such tissues as spleen, liver, kidney, lung, adrenals, and thyroid amounted to only 10-20% of that found in brain. This distribution of enzyme activity, together with its preference for oligopeptides as substrates, its ability to generate leu- and met-enkephalin from several larger peptide precursors, and its affinity toward several other bioactive peptides, suggests that the enzyme functions in the metabolism of neuropeptides.
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PMID:Soluble metalloendopeptidase from rat brain: action on enkephalin-containing peptides and other bioactive peptides. 388 8

Angiotensin II has a major effect on mineralocorticoid hormone synthesis in patients with idiopathic hyperaldosteronism; it has little or no effect in those with an aldosterone-producing adenoma. To determine if this difference could be of use in clinically separating these two forms of primary aldosteronism, saline infusion tests were performed in 20 patients--14 with surgically proved aldosterone-producing adenoma and six with idiopathic hyperaldosteronism. With the patients receiving a balanced diet containing 120 meq of sodium, 1,250 ml of isotonic saline was infused intravenously between 8 A.M. and 10 A.M. after overnight recumbency. Plasma samples were obtained immediately before and after the infusion. Plasma cortisol level decreased appropriately in both groups, but plasma renin concentration decreased only in those patients with idiopathic hyperaldosteronism (p less than 0.05). Aldosterone and 18-hydroxycorticosterone levels decreased in both groups. To account for the circadian variation in adrenocorticotropin levels during the course of saline infusion, 18-hydroxycorticosterone/cortisol and aldosterone/cortisol ratios were examined. Both ratios increased in every patient with aldosterone-producing adenoma (p less than 0.01 and p less than 0.001, respectively), but these ratios remained unchanged or decreased in the patients with idiopathic hyperaldosteronism. This divergent variation in ratios after saline infusion allows for the differentiation of patients with an aldosterone-producing adenoma from those with idiopathic hyperaldosteronism. In patients with primary aldosteronism, an 18-hydroxycorticosterone/cortisol ratio of less than 3.0 or an aldosterone/cortisol ratio of less than 2.2 after saline infusion is diagnostic of idiopathic hyperaldosteronism.
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PMID:Use of the saline infusion test to diagnose the cause of primary aldosteronism. 390 46

The effect of stimulating and suppressive influences on plasma aldosterone in normal man and in patients with primary aldosteronism were studied using a sensitive double-isotope derivative assay for aldosterone. In normal sitting subjects, values were 9.2+/-0.9 (SE) mmug/100 ml and in subjects supine for 1 hr plasma aldosterone was 5.2+/-0.4 (SE) mmug/100 ml. Adrenocorticotropic hormone (ACTH), 0.5 U/hr, produced a rise of 46.8+/-22 (SE) mmug which was similar to the 1-hr effect of an infusion of a synthetic ACTH (beta(1-24), Cortrosyn). Angiotensin II in pressor amounts also increased plasma aldosterone 21.5+/-2.9 (SE) without change in plasma cortisol, whereas a subpressor dose ([unk]) had minimal effect.Fludrocortisone, 1.2 mg/day for 3 days, suppressed plasma aldosterone levels to 1.8+/-0.7 (SE) mmug/100 ml in five normal sitting subjects (P < 0.01); however, dexamethasone, 2 mg/day for 1-2 days, did not lower aldosterone concentration in plasma. In six patients with primary aldosteronism, plasma aldosterone on a normal sodium diet was 39.1+/-4.4 (SE) which differed significantly from normal sitting or supine subjects (P < 0.001). In contrast to the normal subjects, neither a pressor infusion of angiotensin II for 1 hr, nor fludrocortisone, 1.2 mg/day for 3 days, impressively altered plasma aldosterone levels. This approach appears to be useful for the study of the acute physiology and control mechanisms of aldosterone production in normal and hypertensive man.
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PMID:Stimulation and suppression of aldosterone in plasma of normal man and in primary aldosteronism. 430 57

The effects of adrenocorticotropin (ACTH), angiotensins I and II, increased potassium, and decreased sodium concentrations upon steroid synthesis were examined by incubation of beef adrenal tissue slices. Angiotensin II shared with ACTH the need for calcium and an inhibition of its effect in the presence of puromycin but differed in not stimulating cyclic adenosine monophosphate (AMP). Angiotensin I was effective in steroidogenesis. The stimulation of aldosterone synthesis by increased potassium concentration was accompanied by an increased level of cyclic AMP and was inhibited in the presence of puromycin. Decreased sodium concentration stimulated aldosterone synthesis but, alone of these stimuli, simultaneously decreased corticosterone levels. It therefore appears that ACTH and potassium stimulate steroidogenesis at an early step in the biosynthetic pathway through the activation of cyclic AMP, whereas the effect of angiotensins I and II involve another mechanism and decreased sodium concentration affects a later step in steroidogenesis.
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PMID:Adrenocortical steroidogenesis: studies on the mechanism of action of angiotensin and electrolytes. 434 26

We studied the effect of chronic carotid body denervation on renin (plasma renin activity, PRA), adrenocorticotropin (ACTH), blood pressure, and hematocrit responses to acute normocapnic (arterial CO2 partial pressure, PaCO2, 35 Torr) and hypercapnic (PaCO2, 65 Torr) hypoxia (arterial O2 partial pressure, PaO2, 31 Torr) in five anesthetized, artificially ventilated dogs. Animals were studied at least 3 days before and again at least 10 days after carotid body denervation (bilateral carotid sinus nerve resection). Increases in PRA during hypercapnic normoxia [21.8 +/- 6.4 ng angiotensin I (ANG I) X ml-1 X 3 h-1] and normocapnic hypoxia (13.3 +/- 4.2 ng ANG I X ml-1 X 3 h-1) were not attenuated by carotid body denervation. Increases in ACTH during normocapnic hypoxia (117 +/- 34 pg/ml) were attenuated but not eliminated by carotid body denervation; the increase in ACTH during hypercapnic hypoxia (295 +/- 93 pg/ml) was not attenuated by carotid body denervation. Both the blood pressure and hematocrit responses to normocapnic and hypercapnic hypoxia were attenuated by carotid body denervation. We concluded that 1) the renin response to hypercapnia and hypoxia is not a carotid chemoreflex, 2) the ACTH response to hypoxia is partially a carotid chemoreflex, and 3) blood pressure and hematocrit responses to hypoxia are primarily carotid chemoreflexes.
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PMID:Renin and ACTH responses to hypercapnia and hypoxia after chronic carotid chemodenervation. 608 93

The present report concerns the immunocytochemistry of various peptide hormones and in particular their location in nervous structures. However, since the hormones observed in the neuroadenohypophysis and the digestive tractus have been examined elsewhere, they have been excluded from this study, except when considered outside there precise areas. The immunocytology of the following neuropeptides is presented, especially the particular details related to their demonstration: 1) The hypothalamic hypophysiotropic factor: LH-RF, SRIF, TSH-RF; derivatives from the so-called proopiocortine found by Mains and Eipper (1977), namely beta-LPH, enkephalins, endorphins, alpha-MSH- and ACTH-like antigens; 2) Prolactin and somathormone found outside the pituitary; 3) Gastro-intestinal hormones and their location outside the digestive hormones and their location outside the digestive mucosa, namely VIP, CCK, substance P; 4) Angiotensin II in nervous structures; 5) Neurotensin; 6) Thyrocalcitonin; 7) Relaxin, and the problem of its presence in the adult male genital tract. New data in invertebrate located vertebrate neuropeptides-like antigens in the nervous structures of pro-chordates (Ascidians) insects, crustaceans, annelids. These last findings underline the extensive significance of such hormonal molecules previously considered to be specific for vertebrates.
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PMID:Immunocytochemistry of polypeptide hormones: a review. 616 60

We have further characterized angiotensin receptors on bovine adrenal fasciculata cells whose presence was previously demonstrated by the intrinsic agonistic activity of angiotensin II (AII), dex-Asp1-AII, angiotensin I (AI), and des-ASp1-AI on steroidogenesis. The specific binding of AII and des-Asp1-AII labeled with 125I to dispersed bovine fasciculata cells was studied. For both peptides, a single class of binding sites accounted for the data with a mean (+/- SEM) Ka value of 0.23 +/- 0.123 X 10(8) liters/mol for AII and 0.68 X 10(8) liters/mol for des-Asp1-AII. The concentration at which unlabeled AII and des-Asp1-AII displaced 50% of the tracers (Kd) was similar to that at which they induced half-maximal stimulation of steroidogenesis (Kact). For AI and des-Asp1-AI, Kd greater than Kact. Analogs of AII or des-Asp1-AII with antagonistic properties upon steroidogenesis competed also with binding of the tracers. Corticotropin (ACTH) did not inhibit binding. Although ACTH stimulated the formation of cyclic AMP, none of the angiotensins with intrinsic activity did so. Calcium, but not potassium, appeared to potentiate the steroidogenic activity of AII. These data suggest that there is a single class of receptors for angiotensins and analogs in zona fasciculata. These receptors show characteristics that differentiate them from ACTH receptors in zona fasciculata or angiotensin receptors in zona glomerulosa cells.
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PMID:Characterization of angiotensin receptors on bovine adrenal fasciculata cells. 626 51

To investigate the role of non-ACTH pituitary peptides on steroidogenesis, we studied the effects of synthetic beta-lipotropin, beta-melanotropin, and beta-endorphin on aldosterone and corticosterone stimulation using rat adrenal collagenase-dispersed capsular and decapsular cells. beta-lipotropin induced a significant aldosterone stimulation in a dose-dependent fashion (10 nM-1 muM). beta-endorphin, which is the carboxyterminal fragment of beta-lipotropin, did not stimulate aldosterone production at the doses used (3 nM-6 muM). beta-melanotropin, which is the middle fragment of beta-lipotropin, showed comparable effects on aldosterone stimulation. beta-lipotropin and beta-melanotropin did not affect corticosterone production in decapsular cells. Although ACTH(1-24) caused a significant increase in cyclic AMP production in capsular cells in a dose-dependent fashion (1 nM-1 muM), beta-lipotropin and beta-melanotropin did not induce an increase in cyclic AMP production at the doses used (1 nM-1 muM). The beta-melanotropin analogue (glycine[Gly](10)-beta-melanotropin) inhibited aldosterone production induced by beta-lipotropin or beta-melanotropin, but did not inhibit aldosterone production induced by ACTH(1-24) or angiotensin II. Corticotropin-inhibiting peptide (ACTH(7-38)) inhibited not only ACTH(1-24) action but also beta-lipotropin or beta-melanotropin action; however it did not affect angiotensin II-induced aldosterone production. (saralasin [Sar](1); alanine [Ala](8))-Angiotensin II inhibited the actions of beta-lipotropin and beta-melanotropin as well as angiotensin II. These results indicate that (a) beta-lipotropin and beta-melanotropin cause a significant stimulation of aldosterone production in capsular cells, (b) beta-lipotropin and beta-melanotropin have a preferential effect on zona glomerulosa cells, (c) beta-melanotropin contains the active peptide core necessary for aldosterone stimulation, (d) the effects of these peptides on aldosterone production may be independent of cyclic AMP, and (e) the receptors for beta-lipotropin or beta-melanotropin may be different from those for ACTH or angiotensin II.
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PMID:Effects of beta-lipotropin and beta-lipotropin-derived peptides on aldosterone production in the rat adrenal gland. 626 63

Angiotensin II (ANG II) acts on the brain to elevate blood pressure (BP), stimulate drinking, increase the secretion of vasopressin and corticotropin (ACTH), and inhibit the secretion of renin. The present studies were designed to evaluate the possible physiological significance of these effects. The experiments were performed in conscious dogs with small catheters chronically implanted in both carotid and both vertebral arteries. ANG II was infused into both carotid or both vertebral arteries in doses of 0.1, 0.33, 1.0, and 2.5 ng.kg-1.min-1. Intravertebral ANG II produced dose-related increases in BP that were generally accompanied by increases in heart rate. Intracarotid angiotensin also increased BP but did not change heart rate. Intracarotid ANG II stimulated drinking and, at the highest dose only, increased the secretion of vasopressin, ACTH, and corticosteroids. Intravertebral and intracarotid ANG II suppressed plasma renin activity (PRA). In a parallel series of experiments, the effects of intravenous ANG II, in doses of 2, 5, 10, and 20 ng.kg-1.min-1, were studied. These infusions produced dose-related increases in BP and water intake and suppressed PRA. Only the highest dose of ANG II increased vasopressin or corticosteroid secretion. Analysis of these results in terms of calculated or measured changes in plasma ANG II concentration indicate that the central cardiovascular and dipsogenic actions of angiotensin, as well as the suppression of PRA, can be elicited by concentrations of the peptide that are within the physiological range. On the other hand high, probably supraphysiological, levels of ANG II are required to increase vasopressin or ACTH secretion.
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PMID:Analysis of the actions of angiotensin on the central nervous system of conscious dogs. 628 22

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