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

The rat zona glomerulosa has a renin-angiotensin system that appears to function as an autocrine or paracrine system in the regulation of aldosterone production. To further investigate dynamic changes of production of renin and aldosterone in vitro we developed a primary monolayer culture of rat adrenal glomerulosa cells in serum-free medium. Collagenase-dispersed glomerulosa cells were incubated in PFMR-4 medium containing 10% fetal calf serum for 48 hours; the medium was then replaced with serum-free PFMR-4 medium. The cell viability and the aldosterone secretion were stable over the additional 48 hours in the serum-free control medium. After incubation for 24 hours in the serum-free medium, the cells were exposed to high K+ or adrenocorticotropic hormone (ACTH) for another 24 hours. ACTH stimulated aldosterone secretion, and this increased secretion was associated with an increase in renin activity (cell active renin, from 15.56 +/- 0.71 to 45.75 +/- 5.69; cell inactive renin, from 0.67 +/- 0.54 to 8.75 +/- 3.40; medium inactive renin, from 5.58 +/- 1.16 to 106.20 +/- 14.01 pg angiotensin I (Ang I)/micrograms protein/3 hr). Aldosterone was also stimulated by high K+. This increase was also associated with an increase in active renin in the cells (from 15.08 +/- 1.80 to 23.26 +/- 2.15 pg Ang I/micrograms protein/3 hr) and an increase in inactive renin in the medium (from 10.87 +/- 1.62 to 21.37 +/- 3.20 pg Ang I/micrograms protein/3 hr). Addition of the angiotensin converting enzyme inhibitor lisinopril attenuated both ACTH- and high K(+)-stimulated aldosterone secretion significantly.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1990 Dec
PMID:Role of the adrenal renin-angiotensin system on adrenocorticotropic hormone- and potassium-stimulated aldosterone production by rat adrenal glomerulosa cells in monolayer culture. 217 21

Based on the analysis of a RX-ray study and a selective blood test for the activity of the plasma renin, aldesterone, hydrocortisone and adrenocorticotropic hormone (ACTH) in 57 patients with arterial hypertension--14 persons without renal failure, 14 ones regularly treated by hemodialysis, 29 patients with left orthostatic varicocele--the authors demonstrated the impact of the renal arterio- and phlebography on the hormone levels studied. Arteriography resulted in an increase in the absolute value of the renal vein renin mean 2.1-fold, aldosterone, 3.3-fold and hydrocortisone, 1.7-fold. A 2.2-fold increase in the renin activity and a 2.6-fold increase in the levels of aldosterone and hydrocortisone noted in all the patients were the result of retrograde renal phlebography. No correlations were established between the changes in hormone levels and the central mechanism of the secretion regulation (ACTH). Radiopaque investigations of the patients with arterial hypertension gave 22 per cent of false positive results with regard to the site of renin secretion and 18 per cent of those with regard to the participation of the studied kidney in renin secretion. The authors supposed a possible regulation of adrenal mineralocorticoid performance by a retrograde blood flow appeared through the adrenal central veins that was induced by phlebography--related elevation of blood pressure in the renal vein.
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PMID:[The effect of renal arterio- and phlebography on the function of the renin-angiotensin and hypophyseal-adrenal systems]. 218 46

The purpose of this study was to evaluate the effect of clonidine--an alpha 2-adrenergic agonist--and naloxone--an opiate antagonist--on pituitary hormone release. The study involved 43 women: 20 menopausal women, 9 untreated women with ACTH-dependent Cushing's disease, and 14 healthy women. Serum GH, ACTH, LH, FSH, TSH, cortisol, and plasma beta-endorphin concentrations were measured with RIA methods. A significant increase in GH and a significant decrease in ACTH and in cortisol was observed after clonidine injection in healthy women. Clonidine caused a significant decrease in LH concentration in the luteal phase of the menstrual cycle. However, naloxone induced the opposite effect on pituitary hormone release. In Cushing's disease, ACTH significantly decreased in response to clonidine. In postmenopausal women with hypertension a decrease in blood pressure, a marked decrease in the number of hot flashes, as well as a diminution in amplitude and frequency of LH pulsatility was found. Conclusions are as follows: (1) Clonidine may be useful in the treatment of hypertensive menopausal women; and (2) a diminution in ACTH, beta-endorphin, and cortisol release in response to clonidine was observed in Cushing's disease.
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PMID:The effect of clonidine on pituitary hormone secretion in physiological and pathological states. 245 86

An effect of the treatment with guanfacine on the activity of the adreno-sympathetic system, beta-thromboglobulin, beta-endorphin, and blood lipids was studied in 30 patients with the primary arterial blood hypertension. It was found that guanfacine significantly decreases plasma noradrenaline, adrenaline, and dopamine. Moreover, it decreases the excretion of noradrenaline, adrenaline and 4-hydroxy-3-methoxy-phenylglycol. These effects correlate with the drop in both systolic and diastolic blood pressure. A decrease in plasma renin activity was also observed. It correlated with the blood pressure drops. Guanfacine increased beta-endorphin levels while beta-thromboglobulin, total cholesterol and triglycerides levels remained unaffected. The authors suggest that the hypotensive effect of guanfacine is related to the decrease in adreno-sympathetic system activity and plasma renin activity and no effect on the erythrocyte activity and lipids metabolism.
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PMID:[Effect of long-term treatment with guanfacine on selected humoral metabolic indices in patients with primary hypertension]. 253 May 2

Research suggests that heightened cardiovascular and neuroendocrine (typically catecholamine) responses to stressors may lead to the development of hypertension and that there may be race differences in patterns of reactivity that are potentially pathogenic. Certain neuropeptides exert profound effects on blood pressure (BP) and heart rate (HR), yet no published studies have examined relationships between these peptides, hypertensive status, race, and reactivity. Seventeen Black and 20 White normotensive and borderline-hypertensive male 19- to 50-year-olds underwent intravenous catheterization while cardiovascular and neuropeptide responses to the stress of being catheterized were examined. Results indicate that, in response to the stressor, Black hypertensives, showed significantly lower endorphin levels compared to Black normotensives, and White hypertensives showed significantly higher levels of beta-endorphin compared to White normotensives. Groups were not significantly different in endorphin levels at recovery. Black hypertensives also showed significantly higher stressor-induced HR and systolic and diastolic BP compared to White hypertensives and normotensives. Lower levels of beta-endorphin and lower urine sodium excretion were associated with higher BP and HR.
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PMID:Neuropeptide and cardiovascular responses to intravenous catheterization in normotensive and hypertensive blacks and whites. 253 95

The effect of intracisternal pretreatment with opiate antagonists or antisera against various opioid peptides on the hypotension and bradycardia induced by cumulative intracisternal administration of clonidine (0.02-2.5 microgram) was studied in conscious Wistar-Kyoto rats and in spontaneously hypertensive rats. No effect of any pretreatment on basal values of blood pressure and heart rate was detected in either of these strains. In spontaneously hypertensive rats intracisternal pretreatment with naltrexone resulted in a dose-dependent inhibition of clonidine-induced hypotension and bradycardia. DL-naloxone also antagonized the hypotension but not influence the hypotensive and bradycardic response to clonidine. In Wistar-Kyoto rats naltrexone and the beta-endorphin antiserum B4 failed to affect the cardiovascular effects of clonidine. B4 and an antiserum against dynorphin(1-13) inhibited clonidine-induced hypotension in spontaneously hypertensive rats, whereas a [Met5]enkephalin antiserum had no effect. Use of antisera specifically recognizing the C-terminus of beta-, alpha-, and gamma-endorphin, respectively, revealed that only the beta-endorphin antiserum inhibited the fall in blood pressure in spontaneously hypertensive rats after cumulative administration of clonidine. None of the antisera used affected clonidine-induced bradycardia. These results indicate that activation of stereospecific opiate receptors in spontaneously hypertensive, but not in Wistar-Kyoto rats, plays a role in the central hypotensive effect of clonidine. beta-Endorphin(1-31) and dynorphin(1-13) might be the endogenous ligands for these receptors.
Hypertension 1989 Jan
PMID:Possible involvement of brain opioid peptides in clonidine-induced hypotension in spontaneously hypertensive rats. 253 2

Evidence from numerous laboratories has shown that administration of adrenocorticotropic hormone (ACTH) to rats produces hypertension within 5 days. However, the analysis of blood pressure in these studies was by the tail-cuff technique, an acute and indirect approach. We have now administered ACTH, via a subcutaneous depot injection (5 or 10 U/day for 9 days), to chronically instrumented rats maintained in metabolic cages. Although tail-cuff measurements of arterial pressure indicated that the ACTH treatment produced hypertension, this was not confirmed by direct 24-h measurements of mean arterial pressure. There was no effect of ACTH on 24-h heart rate throughout the treatment period compared with saline-injected controls. We also examined coefficient of variation of all our measurements. None of the factors was altered by ACTH administration. However, ACTH treatment did produce a diuretic effect, further confirming previous work and providing renal, in addition to cardiovascular, evidence for the bioavailability of the ACTH depot. These results demonstrate that chronic ACTH treatment does not produce a true hypertensive state in rats but rather may enhance the cardiovascular response to the stress of the indirect arterial pressure measurement technique.
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PMID:ACTH-induced hypertension in rats: fact or artifact? 254 14

An effect of enalapril maleate on the activity of renin-angiotensin-aldosterone system and sympathetic reactivity, erythrocyte prostaglandin and sodium levels as well as blood beta-endorphin was investigated in 28 patients with the essential arterial blood hypertension. It was found that enalapril maleate significantly increased plasma renin activity, decreased plasma norepinephrine and its 24-hour excretion, and decreased erythrocyte beta-endorphin and sodium levels. Blood epinephrine and aldosterone levels and their daily excretion remained unchanged similarly to prostaglandins. The above results suggest that a decrease in sympathetic system activity and intracellular sodium concentration may play a role in the hypotensive action of enalapril maleate related to the inhibition of angiotensin II formation.
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PMID:[Effect of treatment with enalapril maleate on the levels of circulating catecholamines, beta endorphins, prostaglandins, and concentration of sodium in erythrocytes in patients with essential hypertension]. 255 61

Endogenous opioid regulation of blood pressure is altered during stress in young adults at risk for hypertension. We studied the effects of the opioid antagonist naloxone on the secretion of corticotropin and beta-endorphin during psychological stress in young adults with mildly elevated casual arterial pressures. Naloxone-induced secretion of both corticotropin and beta-endorphin was significantly diminished in persons at enhanced risk for hypertension compared with the low blood pressure control group. Results suggest that opioidergic inhibition of anterior pituitary function is altered in hypertension development.
Hypertension 1989 Dec
PMID:Altered pituitary hormone response to naloxone in hypertension development. 255 3

In humans, the syndrome of cortisol resistance is characterized by the absence of signs and symptoms of Cushing's syndrome, elevated total and unbound plasma cortisol concentrations, and increases in urinary free cortisol excretion and plasma adrenocorticotropic hormone. In one family, a severely affected member had hypertension and hypokalemic alkalosis associated with increased plasma concentrations of corticosterone and deoxycorticosterone. These patients are resistant to suppression of the pituitary-adrenal axis by dexamethasone. Dexamethasone therapy, however, effectively corrected hypertension and hypokalemic alkalosis in the severely affected patient, without causing signs of glucocorticoid excess. The glucocorticoid receptor from these patients has a low affinity for glucocorticoids and is unstable during thermal activation. Both the molecular weight of the glucocorticoid receptor and the size of the corresponding mRNA are similar to those of normal controls. Transformation of B-lymphocytes with Epstein-Barr virus leads to induction of glucocorticoid receptors. Receptor induction, however, is lower in patient cells than those obtained from normal controls. This decreased induction parallels decreased expression of glucocorticoid receptor mRNA. Thus, in this form of glucocorticoid resistance the glucocorticoid receptor is abnormal and leads to diminished target organ responsiveness. Many New World primates exhibit glucocorticoid "resistance," without apparent pathology. These species have markedly elevated plasma cortisol, both total and unbound concentrations, increased urinary free cortisol excretion, and marked increases in plasma adrenocorticotropic hormone and beta-endorphin. The glucocorticoid receptors of these primates have decreased affinity for glucocorticoids, are thermolabile, and are not induced by Epstein-Barr virus transformation as indicated by specific binding and mRNA expression. Both the molecular weight of the glucocorticoid receptor and the size of the corresponding mRNA are similar to those of normal controls. Despite the high plasma cortisol concentrations in these primates, there is no sodium retention and aldosterone levels are actually increased. The kidney aldosterone receptor cross-reacts poorly with cortisol, explaining the absence of sodium retention. New World primates also have progesterone, estrogen, aldosterone, and vitamin D insensitivity, suggesting a common factor linking steroid hormone receptors.
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PMID:Glucocorticoid resistance in humans and nonhuman primates. 264 36


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