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

In order to evaluate the role of beta-endorphin in the pathogenesis of obesity and essential hypertension 44 subjects were investigated: 12 nonobese hypertensives, 11 obese hypertensives, 11 obese normotensives and 10 normal subjects. Plasma concentrations of beta-endorphin and cortisol were measured by radioimmunological and ACTH by immunoradiometric methods. The plasma concentrations and the circadian rhythms of ACTH and cortisol secretion were normal in all groups investigated. A circadian rhythm of beta-endorphin secretion was demonstrated in nonobese hypertensives and in normal subjects. The plasma concentrations of beta-endorphin were twice higher than those in nonobese subjects. Also, in all obese patients the circadian rhythm of beta-endorphin secretion was blunted. The increased concentrations and the altered circadian rhythm of beta-endorphin in all obese subjects may point to a role of beta-endorphin in the pathogenesis of obesity rather than in that of essential hypertension.
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PMID:The possible role of beta-endorphin in pathogenesis of obesity and essential hypertension. 283 3

The effects of ovine corticotropin releasing factor (o-CRF) on plasma aldosterone, 18-OH-corticosterone (18-OHB), plasma adrenocorticotropin (ACTH) and cortisol were determined in eight patients with primary aldosteronism, six with aldosterone-producing adenoma (APA) and two with idiopathic hyperaldosteronism (IHA). The results were compared with those in six normal subjects and eleven patients with essential hypertension (EHT, 5 with low renin and 6 with normal renin). In patients with APA, the peak plasma aldosterone and 18-OHB responses to 100 micrograms iv of o-CRF (226% and 113% increase from baseline, respectively) were greater than those in EHT and normal subjects. The net integrated aldosterone and 18-OHB responses (840 +/- 156, and 419 +/- 121 ng/dl.hr, respectively) were also significantly greater (p less than 0.01) in APA than those in normals and EHT. In two patients with IHA, both the peak and net integrated aldosterone response were smaller than those in APA, in spite of nearly identical plasma ACTH and cortisol responses. These results suggest that augmented responses of mineralocorticoids to o-CRF may be characteristic of aldosteronism due to APA, mediated by CRF-induced ACTH, and possibly other proopiomelanocortin (POMC)-derived peptides.
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PMID:Effects of corticotropin-releasing factor (CRF) on aldosterone and 18-hydroxycorticosterone in essential hypertension and primary aldosteronism. 283 82

The role of alpha 2-adrenoceptor stimulation by clonidine on the secretion of beta-endorphin, ACTH, and cortisol in essential hypertension and obesity was studied in 45 subjects: 15 non-obese hypertensives, 10 obese hypertensives, 11 obese normotensives, and 9 healthy subjects. The circadian rhythm of plasma beta-endorphin, ACTH, and cortisol was determined after placebo and after three days on clonidine 0.45 mg daily. Clonidine lowered the blood pressure and blood ACTH and cortisol levels in all the subjects. A significant decrease in beta-endorphin after clonidine occurred in the healthy subjects. In obese normotensives basal beta-endorphin concentrations were significantly higher than in healthy subjects and did not change after clonidine. In about 50% of non-obese and obese hypertensives a significant increase in beta-endorphin secretion after clonidine was noted (responders). In the subgroup of non-obese hypertensive responders no circadian rhythm of beta-endorphin was observed. The results suggest that adrenergic regulation of beta-endorphin secretion is altered in obesity and in certain patients with essential hypertension.
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PMID:Effect of clonidine on beta-endorphin, ACTH and cortisol secretion in essential hypertension and obesity. 284 28

In young men with mild essential hypertension and age-matched normotensive volunteers, plasma concentrations of the endogenous opioid beta-endorphin were determined hourly from 9:00 p.m. to 2:00 a.m. The hypertensive patients' mean plasma beta-endorphin concentration was significantly lower in comparison with normotensive controls. After 14 days of treatment with clonidine, systolic and diastolic blood pressure was significantly reduced in both groups. Plasma beta-endorphin concentration increased in the hypertensive patients, but remained unchanged in the normotensive volunteers. The present findings point to a possible involvement of reduced beta-endorphinergic activity in blood pressure regulation of young men with essential hypertension.
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PMID:Clonidine normalizes low plasma beta-endorphin concentration and blood pressure in young men with mild essential hypertension. 294 42

In a randomized, double-blind crossover study 13 untreated patients with mild essential hypertension were exposed to submaximal bicycle exercise. Sixty minutes before ergometry 10 mg metoclopramide or placebo, and 10 min before exercise 0.4 mg naloxone or placebo, were given intravenously. Plasma adrenocorticotrophic hormone, beta-endorphin and cortisol levels increased significantly after ergometry, whether performed after placebo, naloxone, metoclopramide or metoclopramide + naloxone treatment. However, only naloxone administration potentiated plasma adrenocorticotrophic hormone, beta-endorphin and cortisol responses to workload. Plasma levels of adrenocorticotrophic hormone, beta-endorphin and cortisol were 45 +/- 14 pg/ml, 6.2 +/- 1.2 pmol/l and 141 +/- ng/ml, respectively, after ergometry, when performed after placebo, but these values were increased to 61 +/- 10 pg/ml, 11.4 +/- 2.8 pmol/l and 207 +/- 22 ng/ml, respectively, after naloxone treatment. This naloxone-induced potentiation of hormonal release was blocked by metoclopramide pretreatment, suggesting a close interaction between dopaminergic and opioidergic mechanisms, regulating hormonal responses to physical exercise.
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PMID:Dopaminergic-opioidergic interaction is reflected by changes in pituitary hormone secretion in patients with essential hypertension. 297 77

Excessive production of an as yet unidentified aldosterone-stimulating factor may cause idiopathic hyperaldosteronism (IHA). This putative factor may be related to proopiomelanocortin-derived peptides, some of which have aldosterone-stimulating properties. The present study evaluated plasma beta-endorphin, ACTH, cortisol, and aldosterone levels in patients with IHA (n = 10), aldosterone-producing adenomas (n = 4), essential hypertension (n = 11), and normal subjects (n = 10). Plasma and urinary hormone measurements were obtained at timed intervals during an isocaloric, fixed electrolyte intake (Na+, 128 meq/day; K+, 80 meq/day) in a metabolic unit. Plasma for beta-endorphin assay was preincubated with sepharose-bound anti-beta-lipotropin to remove beta-lipotropin that cross-reacted with the beta-endorphin RIA. Mean +/- SE plasma beta-endorphin levels at 0800 h were elevated in IHA patients (47 +/- 13 fmol/ml) compared to those in aldosterone-producing adenoma (25 +/- 9), essential hypertension (16 +/- 1), and normal control (20 +/- 2; P less than 0.05) subjects. Plasma ACTH, plasma cortisol, and urinary cortisol levels were not different in these four groups. These data support the hypothesis that excess production of either beta-endorphin or related proopiomelanocortin-derived peptides may function as aldosterone secretogogue(s) in IHA.
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PMID:Plasma beta-endorphin levels in primary aldosteronism. 298 Dec 43

Results of supraphysiological adrenocorticotropic hormone (ACTH) stimulation of biosynthetic pathways of adrenal zona fasciculata indicate that a deficiency of 11-hydroxylase exists in patients with essential hypertension. The deficiency is suggested by the much greater stimulus of synthesis of deoxycorticosterone (DOC) and deoxycortisol in hypertensive subjects than in controls (p less than 0.001). No significant difference in the synthesis of cortisol, corticosterone, progesterone, 17-hydroxyprogesterone (17-OHP), and delta-4-androstenedione (D4) was observed between the two groups. The ratios for synthesis of DOC and corticosterone and for deoxycortisol and cortisol found in hypertensive patients were significantly higher than those found in controls (p less than 0.001); no significant difference was observed in the synthesis of 17-OHP and progesterone. The synthesis of DOC and deoxycortisol was not significantly correlated with either blood pressure or plasma renin activity. Plasma renin activity was significantly lower in hypertensive subjects than in normotensive subjects (p less than 0.0001), while no difference was found in aldosterone secretion between the two groups. The 11-hydroxylase deficiency in the adrenal zona fasciculata may be one of the genetic factors causing hypertension together with environmental factors (particularly salt intake and work-related stress). The investigation performed in our study may be useful for the evaluation of adrenal zona fasciculata enzymatic activities during the study of hypertensive patients.
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PMID:Partial deficiency of adrenal 11-hydroxylase. A possible cause of primary hypertension. 298 17

The authors studied the effect of adrenocorticotropic hormone (ACTH), potassium and plasma renin activity on blood aldosterone in normal subjects as well as in patients with essential hypertension (of a labile and stable course) and hyperaldosteronism (primary and idiopathic). It was demonstrated that in normal subjects and patients with labile essential hypertension, the secretion of aldosterone was simultaneously stimulated by the renin-angiotensin system (RAS) and the hypothalamus-adenopituitary. The RAS dominated in normal conditions whereas in labile hypertension the hypothalamus-adenopituitary system was predominant. In stable hypertension, the RAS and hypothalamus-pituitary influenced aldosterone secretion in an equal degree. Hyperaldosteronism was associated with the most pronounced deviations in the relationship between stimulants and aldosterone. In addition to decreased plasma levels of renin activity and potassium, the corticotropic activity of the hypothalamus-adenopituitary was increased during the first 10 years of the disease, while later on the function of this system became inhibited. The highest ACTH levels were recorded in idiopathic hyperaldosteronism.
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PMID:[Concentration of adrenocorticotrophic hormone and aldosterone secretion in essential hypertension and hyperaldosteronism]. 298 49

Whether peripheral beta-endorphin contributes to the antihypertensive action of clonidine was examined by measuring plasma levels of beta-endorphin-like immunoreactivity (beta EpLI) after acute administration of clonidine in patients with essential hypertension. Administration of clonidine (0.225 mg) in one dose significantly lowered blood pressure, decreased heart rate and reduced the plasma level of beta EpLI and ACTH, while the placebo had no effect on blood pressure, heart rate or plasma level of beta EpLI suggesting that peripheral beta-endorphin does not play a major role in the antihypertensive action of acute clonidine administration.
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PMID:Central alpha-activation by clonidine reduces plasma level of beta-endorphin in patients with essential hypertension. 299 46

Analysis of the effect of naloxone (0.4 mg iv.) on clonidine hypotension in 80 patients with essential hypertension revealed that two groups could be separated. In the responding group (43 pts) naloxone increased blood pressure and heart rate in clonidine-treated patients while in the non-responding group (37 pts) it has no such effect. Patients in the responding group had higher cardiac output, stroke volume, plasma renin activity, plasma adrenaline and beta-endorphin levels and lower total peripheral resistance, shorter history of hypertension and lesser body weight than those in the non-responding group. The pressor effect of naloxone in four responding patients treated with clonidine for 29 months tended to be smaller compared to the response obtained after a 3-day clonidine therapy. Results favour the hypothesis of the existence of two (responding, non-responding) groups of patients with essential hypertension. Further work will clarify whether these groups represent different pathogenesis or they indicate only a different stage of hypertension.
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PMID:beta-Endorphin and essential hypertension: importance of the clonidine-naloxone interaction. 315 94


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