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)

Several forms of the polypeptide atrial natriuretic factor (ANF) have been isolated recently from rat and human atria and identified; they are probably associated with the secretory granules of atrial tissue. The potent ability of ANFs to increase urine sodium content is mediated by their direct action on the kidney. We report here the high intrinsic activity of a synthetic replicate of one form of this molecule, ANF(8-33)(ref. 7), to inhibit directly basal aldosterone secretion and its ability to antagonize the stimulatory effects of adrenocorticotropin (ACTH) and angiotensin II (AN-II) on the secretion of aldosterone by rat adrenoglomerulosa cells in vitro. Our results suggest that ANF is of clinical importance in the management of aldosterone-dependent hypertension by modifying the adrenocortical response to endogenous ACTH and AN-II.
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PMID:Inhibition of aldosterone production in the adrenal glomerulosa by atrial natriuretic factor. 609 16

The aldosterone response to adrenocorticotropic hormone (ACTH) and angiotensin II (AII) was evaluated in patients with pituitary insufficiency before and after dietary sodium restriction (10 mEq Na+/day for 12 days). On normal sodium intake, plasma aldosterone concentration and plasma cortisol concentration failed to change from control levels in response to a single injection of ACTH or to a continuous 1-hour infusion of AII in patients with pituitary insufficiency. In response to dietary sodium restriction for 12 days, plasma renin activity (PRA) increased fivefold in patients with pituitary insufficiency, while plasma aldosterone concentration failed to increase significantly, averaging 11.0 +/- 3.1 before and 12.3 +/- 3.7 ng/dl (ns, p greater than 0.05) after sodium deficiency. Although aldosterone secretion failed to increase during sodium deficiency, the patients came into balance at 10 mEq without a significant change in arterial blood pressure (BP). In sharp contrast to the lack of aldosterone response to ACTH before sodium deficiency, plasma aldosterone concentration increased markedly from 12.9 +/- 3.3 to 156 +/- 17.3 ng/dl (p less than 0.001) in response to ACTH after sodium deficiency. Although the adrenal glomerulosa cells were markedly sensitive to ACTH during sodium deficiency, they remained almost totally refractory to AII since aldosterone secretion failed to increase significantly in response to continuous infusion of a pressor dose of AII for 1 hour. Replacement therapy with ACTH gel for 3 months in patients with pituitary insufficiency failed to restore a normal aldosterone response to either ACTH or AII. These data demonstrate that some non-ACTH pituitary factor(s) is essential for a normal aldosterone response to ACTH, AII, and sodium deficiency.
Hypertension
PMID:Regulation of aldosterone biosynthesis during sodium deficiency. Evidence for an essential role of the pituitary gland. 626 60

1. Immunoreactive beta-endorphin (IR-beta EP) was two- to three-fold higher in pituitary neuro-intermediate lobes (N-IL) of spontaneously hypertensive rats (SHR) than of normotensive Wistar--Kyoto (NT-WKY) controls. 2. Plasma levels of IR-beta EP were lower in SHR than in NT-WKY rats. 3. Intravenous injections of morphine lowered blood pressure of both SHR and NT-WKY rats to the same level; naloxone restored blood pressure of both groups to pre-morphine values. 4. Infusion of bromocriptine in SHR for 1 week lowered blood pressure and N-IL IR-beta EP concentration. 5. These results confirm and extend postulated dopaminergic defect in this model of hypertension.
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PMID:Effects of bromocriptine on blood pressure and plasma beta-endorphin in spontaneously hypertensive rats. 627 77

To study the relative roles of sodium (Na+) and calcium ions (Ca2+) in the response of adrenal glomerulosa cells, we investigated the effects of different Na+ concentrations in the incubation media and the actions of substances that interfere with Ca2+ fluxes. Basal aldosterone secretion and response to angiotensin II (AII), adrenocorticotropic hormone (ACTH), or potassium (K+) were dependent on extracellular Na+ concentration. Veratridine, a Na+ channel opener that dissipates Na+ gradients, blocked the stimulated steroidogenic response. Mersalyl acid and tetracaine, which are potent Ca2+ antagonists, blocked the effects of aldosterone secretagogues. Divalent cations with Ca2+ antagonistic action such as manganese M(n2+), nickel (Ni2+), and cobalt (Co2+) blocked the aldosterone secretory response to AII, ACTH, and K+. Barium (Ba2+) and strontium (Sr2+), known to mimick Ca2+ effects, increased or did not affect responses of the glomerulosa cells. Sodium vanadate, an inhibitor of ATP-dependent Ca2+ translocation, did not alter the stimulated aldosterone responses. Trifluoperazine (10(-6) M), an inhibitor of calmodulin, blocked AII and K+-induced aldosterone secretion, but was partially effective on ACTH-stimulated aldosterone output only at a concentration of 10(-5) M. The actions of ouabain on aldosterone biosynthesis were similarly affected by all these drugs. Thus, both extracellular Na+ and Ca2+ appear to play a role in the steroidogenic response of isolated glomerulosa cells. The intracellular action of Ca2+ may involve a calmodulin-like protein. The effects of ACTH are only partially dependent on Ca2+ as a second intracellular messenger.
Hypertension
PMID:Relative roles of sodium and calcium ions in the steroidogenic response of isolated rate adrenal glomerulosa cells. 627 6

Beta-endorphin and related opioid peptides are neuropeptides which appear to play a role in cardiovascular regulation which is supported by altered nociceptive responsiveness in hypertensive animals. In spontaneously hypertensive rats the pain threshold for electric stimulation is elevated; these rats show increased response latency time in a hot plate test. The opiate antagonist naloxone reverses these values to that of the normotensive controls. In other forms of experimental hypertension, eg, renal hypertension (one-clip, two-kidney model), no change in pain sensitivity is apparent. Sinoaortic baroreceptor denervation causes a labile hypertension without changes in hot plate response. Administration of beta-endorphin into the nucleus of the solitary tract (NTS) gradually decreases blood pressure and heart rate without affecting respiratory frequency. These cardiovascular effects are blocked by naloxone as well as by an antibody to beta-endorphin. In contrast to the effects of beta-endorphin, microinjection of enkephalins into the NTS increases blood pressure and heart rate. The data suggest the existence of two separate endorphin systems at the level of the NTS, one a depressor and another a pressor system. The depressor influence of beta-endorphin may play a role in the mechanism of action of antihypertensive agents such as methyldopa and clonidine. Our data support a role of endorphins as neuropeptides involved in cardiovascular regulation, exerting a dual influence at the level of the NTS.
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PMID:Role of opioid peptides in brain mechanisms regulating blood pressure. 629 7

A dopaminergic mechanism has been proposed to suppress aldosterone secretion. To assess the possibility that a defect in the dopaminergic mechanism might enhance aldosterone secretion in hypertensive patients, we determined basal and adrenocorticotropic hormone (ACTH)-stimulated plasma aldosterone (PA), cortisol, renin activity, and potassium concentrations before and during dopamine receptor stimulation with dopamine infusion and bromocriptine administration and dopamine receptor blockade with metoclopramide. The patient study groups included: (a) seven patients with low-renin hypertension and abnormal aldosterone suppression with sodium loading and presumed bilateral zona glomerulosa hyperplasia (ZGHP); (b) two patients with aldosterone-producing adenoma; (c) five patients with low-renin hypertension but normal aldosterone suppression with sodium loading; and (d) six patients with normal-renin hypertension. Dopamine infusion in patients with ZGHP caused PA to fall (P less than 0.01) into the normal range, but did not block the enhanced (P less than 0.05) aldosterone response to ACTH that is characteristic of these patients. Dopamine infusion in patients with low-renin hypertension but normal aldosterone suppression also suppressed PA (P less than 0.01), whereas it had no effect upon PA in patients with normal-renin hypertension or aldosterone-producing adenoma and did not blunt the PA response to ACTH in either group. Bromocriptine administration had no effect upon basal or ACTH-stimulated PA. Dopamine infusion in patients with ZGHP also enhanced (P less than 0.05) diuresis and natriuresis in comparison with normal-renin patients. Metoclopramide administration increased (P less than 0.01) PA in all patients. Thus, a dopaminergic mechanism appears to be important in the regulation of aldosterone secretion in patients with ZGHP and in other low-renin hypertensives with normal aldosterone suppression with sodium loading. In contrast, this latter group does not exhibit an enhanced aldosterone response to ACTH. Both of these groups differ from normal-renin hypertensives, who have no PA suppression with dopamine infusion.
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PMID:Aldosterone suppression with dopamine infusion in low-renin hypertension. 630 9

A 7-year-old girl presented with the physical and endocrinological stigmata of Cushing's disease. An adrenocorticotropic hormone (ACTH)-producing pituitary microadenoma was excised. Three weeks after trans-sphenoidal adenomectomy, the patient developed benign intracranial hypertension. Although ACTH levels had decreased to normal, the serum cortisol had fallen to subnormal levels. The child responded to exogenous steroid therapy, which was gradually tapered and discontinued after 5 months. Normal pituitary and adrenal functions persist 2 years later.
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PMID:Cushing's disease in childhood: benign intracranial hypertension after trans-sphenoidal adenomectomy. Case report. 631 Apr 37

Clinical and biochemical findings in 13 patients (11 women and 2 men) with macronodular adrenocortical hyperplasia (MNH; nodule size, greater than 0.5 to 5.3 cm) were compared with those of 18 patients (15 women and 3 men) with Cushing's disease and diffuse (n = 9) or micronodular (n = 9) hyperplasia (DH). All were bilaterally adrenalectomized for their hypercorticism. The clinical picture was almost identical in both groups, except for greater frequency of hypertension (13 of 13 vs. 10 of 18; P less than 0.05), alopecia (4 of 11 vs. 0 of 15; P less than 0.05), and scintigraphic lateralization (6 of 7 vs. 1 of 7; P less than 0.05) in the MNH group than in the DH group. The sella turcica was enlarged in 30% of the patients in both groups. Patients with MNH were significantly older than DH patients [43.5 +/- 7.8 (mean +/- SD) vs. 31.7 +/- 10.1 yr; P less than 0.005] and had a 3-fold longer duration of disease (7.8 +/- 4.6 vs. 2.0 +/- 1.1 yr; P less than 0.001) than those with DH. The mean plasma ACTH and cortisol levels and urinary 17-hydroxycorticosteroid excretion were elevated in both MNH and DH patients and responded similarly to specific (corticotropin-releasing hormone and metyrapone) and nonspecific (TRH and LHRH) stimuli. However, dexamethasone suppressibility and the stimulatory effect of ACTH on adrenocortical function were less in the MNH than in the DH group or its subgroups, suggesting a greater degree of adrenal autonomy in the former. Adrenal weight in MNH (15.8 +/- 12.1 g each) was almost twice as high as in DH (8.2 +/- 2.0 g) patients and positively correlated with the duration of the disease. The data suggest that MNH may be a result of long-standing Cushing's disease with varying degrees of pituitary dependence and adrenocortical autonomy, which may lead to confusing biochemical and radiological findings. Bilateral adrenalectomy, rather than hypophysectomy, is the treatment of choice in MNH.
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PMID:Macronodular adrenocortical hyperplasia in long-standing Cushing's disease. 631 61

Reported are the concentrations of beta-endorphin, beta-lipotropin, and adrenocorticotropic hormone (ACTH) in the amniotic fluid and plasma of 40 healthy pregnant women at different stages of gestation. Moreover, the amniotic fluid levels of the three peptides were evaluated in 20 other pregnant women affected by different pathologic conditions (Cooley's disease, gestosis, diabetes, placental insufficiency, etc.). A silicic acid extraction procedure was performed on the samples. Each extract was subjected to Sephadex G-75 column chromatography, and the two fractions corresponding to beta-lipotropin and beta-endorphin were collected, freeze-dried, and assayed by two specific radioimmunoassays. Levels of ACTH were measured by radioimmunoassay directly on the extracts. Levels of beta-endorphin in amniotic fluid showed the highest values in the first trimester (173 +/- 30 fmol/ml, mean +/- SEM) but were significantly decreased in the second (75.2 +/- 14) and third trimesters (14.3 +/- 1.8). An inverse trend characterized plasma levels of beta-endorphin, which showed a progressive increase from the first trimester to term (10.4 +/- 11.1). Amniotic fluid levels of beta-lipotropin remained stable during the first (48.6 +/- 6.3) and second (54.6 +/- 11.1) trimesters, but decreased significantly in the third trimester (17.9 +/- 2.3). The plasma concentrations of beta-lipotropin showed the highest levels in the first trimester (10.9 +/- 0.9), and decreased significantly at term (8.9 +/- 1.3). Last, amniotic fluid levels of ACTH decreased from 55.3 +/- 4.75 fmol/ml in the first trimester to 12.5 +/- 1.16 in the second trimester, and rose again in the third trimester to 34.4 +/- 6.6 fmol/ml. Plasma levels of ACTH were characterized in the first two trimesters by values twice those recorded for nonpregnant women, and decreased at term to 8.9 +/- 1.4 fmol/ml. In the pregnant patients with fetuses affected by Cooley's disease (second trimester) and in those with edema-proteinuria-hypertension (EPH) gestosis (third trimester), amniotic fluid levels of beta-endorphin, beta-lipotropin, and ACTH were in the same range as those in healthy pregnant women.
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PMID:Lack of correlation between amniotic fluid and maternal plasma contents of beta-endorphin, beta-lipotropin, and adrenocorticotropic hormone in normal and pathologic pregnancies. 631 61

This report describes a 63-yr-old man with lung cancer accompanying hypertension, hyperpigmentation, muscle weakness, psychosis, hypokalemia, hyperglycemia, hyponatremia, massive natriuresis and lower serum osmolality than urine osmolality. Elevated levels of plasma and urine corticosteroids and of plasma immunoreactive adrenocorticotropic hormone (ACTH) were not altered by the administration of large amounts of dexamethasone. Elevated plasma antidiuretic hormone (ADH) values were also demonstrated. Postmortem examinations revealed small cell lung carcinoma with extensive metastasis, bilateral adrenocortical hyperplasia and Crooke's degeneration of the pituitary gland. Immunoradiological and immunohistochemical studies demonstrated the presence of immunoreactive ACTH, ADH and gastrin-releasing peptide in the tumor tissue. Beta-melanocyte-stimulating hormone, calcitonin and carcinoembryonic antigen were also detected by one of the methods. Hence, this is a rare case of lung cancer with multiple hormone production and clinical and laboratory evidence of both the ectopic ACTH and ADH syndromes.
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PMID:Small cell lung carcinoma with ectopic adrenocorticotropic hormone and antidiuretic hormone syndromes: a case report. 632 89


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