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)

The intravenous (IV) infusion of angiotensin II (AII) was administered to seven healthy male volunteers in a randomized placebo-controlled study. As expected, AII induced a significant increase in blood pressure and plasma aldosterone concentrations. AII caused a significant increase in corticotropin (ACTH) and growth hormone (GH) release, but had no effect on the release of thyrotropin (TSH) and prolactin (PRL). These findings suggest that peripherally circulating AII might influence ACTH and GH secretion in humans.
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PMID:Stimulation of growth hormone and corticotropin release by angiotensin II in man. 217 Aug 20

In order to elucidate whether pituitary peptides other than ACTH which are derived from the proopiomelanocortin (POMC) are involved for aldosterone secretion in primary aldosteronism, we administered ovine corticotropin releasing factor (CRF), beta-endorphin and naloxone to seven patients with aldosterone producing adenoma. One hundred micrograms of CRF produced an augmented aldosterone response in patients with aldosteronism, while 500 micrograms of beta-endorphin infusion failed to cause any significant changes in neither normal subjects nor patients. An opioid antagonist, naloxone (10 mg, iv) produced no noticeable change in plasma aldosterone in normal subjects, while it caused a slight increase in patients with primary aldosteronism. Plasma cortisol increased to a similar degree in response to CRF and naloxone in normal subjects and patients. In three patients with isolated ACTH deficiency, neither aldosterone nor cortisol responded to these stimuli. The present results indicate that POMC-derived pituitary peptides other than ACTH are unlikely to participate in the aldosterone secretion in normal subjects or in patients with primary aldosteronism.
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PMID:Pituitary peptides other than ACTH may not be aldosterone secretagogue in primary aldosteronism. 217 3

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)
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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

In addition to its effect of inhibiting adrenocorticotropic hormone (ACTH) secretion, cortisol (hydrocortisone) inhibits the renin-angiotensin system in both fetal and adult sheep. We have found that progesterone attenuates the inhibition of ACTH by cortisol. These studies test whether progesterone interacts with cortisol in control of the renin-angiotensin-aldosterone system. Conscious adult ewes were infused with vehicle, cortisol (4 micrograms.kg-1.min-1), progesterone (0.5 microgram.kg-1.min-1), or cortisol with progesterone for 60 min. Beginning 120 min after the start of the infusion, renin secretion was stimulated by infusing sodium nitroprusside (10 micrograms.kg-1.min-1 iv). Cortisol infusion decreased plasma K+ concentration and reduced the plasma renin activity (PRA) and aldosterone responses to nitroprusside. Progesterone alone had no effect on PRA, aldosterone, or K+. Progesterone reduced the inhibition of PRA, but not aldosterone or K+, by cortisol. The data also indicate that the suppression of renin, as well as the suppression of ACTH, involves receptors or intracellular mechanisms with which progesterone interacts, whereas the inhibition of aldosterone involves a mechanism that progesterone does not affect.
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PMID:Progesterone-cortisol interaction in control of renin activity but not aldosterone. 220 Dec 19

There are indications that the intermediate lobe peptide alpha-MSH is involved in the regulation of the hydromineral balance in mice and other mammals. The purpose of our studies was to determine whether manipulation of this balance in the mouse could lead to changes in either the rate of POMC biosynthesis in the pars intermedia or to changes in the direction of the processing of the precursor protein to form bioactive peptides. The results show that excess drinking, induced by substitution of drinking water by a 5% glucose solution, causes a rapid increase in POMC synthesis, whereas dehydration has the opposite effect; no evidence could be found that the above treatments have any effect on the processing of POMC, although strain differences were found in level of N-terminal acetylation of newly synthesized melanotropins and endorphins. The changes in various parameters of the hydromineral balance of the animals are consistent with the concept that peptides of the pars intermedia may be involved in regulating plasma aldosterone levels under severe conditions of low plasma sodium concentration.
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PMID:Biosynthetic response of mouse intermediate pituitary gland to induced drinking and dehydration. 233 36

This paper discusses hormonal and metabolic reactions of healthy volunteers exposed to 14-day starvation. This exposure led to many-fold increase of plasma and urinary epinephrine (E); drastic increase of ACTH and beta-endorphin (BE), morning and integrated concentrations of cortisol and STH, aldosterone, T3, glucagon, cAMP, cGMP, cAMP-cGMP, acetyl choline (AC), free fatty acids (FFA), lactate, metanephrine (MN) excretion; decrease of plasma norepinephrine (NE) and unchanged NE excretion; decrease of plasma concentrations of TTH, T4, T3, prolactin (PL), insulin (morning and integrated concentrations), C-peptide, FSH, LH, testosterone, histamine, prostaglandins (PG) A + E, PG F2, glucose and pH, as well as decrease of excretion of homovanillic acid (HVA), vanillyl mandelic acid (VMA), normetanephrine (NMN) and MN-E, NMN:NE. On recovery day 14 concentrations of E, NE, BE, STH, AC, cAMP, cGMP, FFA as well as E and dopamine excretion remained elevated while concentrations of T3, PL, FT, LT, testosterone PG A + E, PG 2 and excretion of MN, HVA, VMA, MN:E remained decreased, while other parameters returned to the normal.
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PMID:[Hormonal and metabolic reactions in the human body during prolonged starvation]. 237 73

Ten patients were studied before and after autologous adrenal medullary transplantation to the central nervous system for Parkinson's disease to determine if the presence of new catecholamine-producing tissue near the hypothalamus would alter hypothalamic or pituitary function, mineralocorticoid levels, or catecholamine production. No clinically apparent ill effects occurred. Changes in endocrine function were largely short-term and transient: at 7-10 days after surgery, urinary catecholamine levels were significantly increased, PRL levels were significantly elevated despite markedly increased serum dopamine levels, and gonadal steroid levels (estradiol and testosterone) were significantly lower despite unchanged basal and stimulated levels of gonadotropins. Dehydroepiandrosterone sulfate was significantly reduced at 7-10 days after surgery and remained low at 3-6 months. Other changes at 3-6 months after surgery included increased stimulated corticotropin levels and reduced serum aldosterone response to upright posture. The changes at 7-10 days were probably due to stress or unilateral adrenalectomy or both; the changes at 3-6 months were likely due to unilateral adrenalectomy. We conclude that unilateral adrenalectomy and autologous adrenal medullary transplantation to the central nervous system does not produce clinically important changes in endocrine function; however, possible adverse consequences of long-term reduction of dehydroepiandrosterone sulfate levels cannot be excluded.
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PMID:Changes in endocrine function after adrenal medullary transplantation to the central nervous system. 239 80

Somatostatin (SRIF) is a potent inhibitor of angiotensin II (AII)-stimulated aldosterone production in rat adrenal glomerulosa cells. This inhibition can be prevented by pretreatment of the cells with pertussis toxin, but little else is known about either the specificity or the biochemical bases of SRIF action in this tissue. We therefore conducted detailed studies of the influence of SRIF on steroidogenesis elicited by AII and the other two physiological stimuli of aldosterone production, K+ and adrenocorticotropic hormone (ACTH), in rat adrenal glomerulosa cells. We also determined the effects of SRIF on cytosolic calcium concentration ([Ca2+]i) and cellular cAMP levels. In these studies, SRIF was found to inhibit the aldosterone responses elicited by low concentrations of all three stimuli, which are believed to promote steroid secretion via discrete but interacting cellular signalling mechanisms. In addition, SRIF consistently lowered cellular cAMP levels in the presence of each of the three agents. However, SRIF caused a small and transient increase rather than a decrease in basal ([Ca2+]i), and had no effect on the subsequent elevation of ([Ca2+]i) by AII and K+. These data indicate that activation of a Gi-like protein by SRIF influences steroid responses to all three major regulators of glomerulosa-cell function, and suggest that basal levels of cAMP play a facilitatory or permissive role in the control of aldosterone production by predominantly calcium-mobilizing regulators of mineralocorticoid secretion.
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PMID:Inhibitory actions of somatostatin on cyclic AMP and aldosterone production in agonist-stimulated adrenal glomerulosa cells. 248 36

We investigated the possibility that angiotensin II (ANGII) augments the sensitivity of the pituitary to corticotropin releasing factor (CRF) by comparing, in patients with essential hypertension, the responses of plasma adrenocorticotropic hormone (ACTH), cortisol, aldosterone, and renin activity to a bolus injection of either 0.5 or 1.0 microgram/kg of synthetic ovine CRF in control conditions and after chronic treatment with the converting enzyme inhibitor captopril to block the formation of ANGII; the effects of CRF were examined up to 4 h after its administration. In control studies, we found that the two doses of CRF induced similar increments in ACTH and cortisol, the levels of which remained elevated throughout the studies; these changes were associated with increments in plasma aldosterone that were dose dependent, less pronounced, and of shorter duration and with a slight decrease in plasma renin activity. Captopril treatment increased basal plasma renin activity and lowered plasma aldosterone while leaving basal ACTH and cortisol unchanged. During converting enzyme inhibition, the responses of ACTH and cortisol to CRF were similar to those observed in control studies, whereas the changes in plasma aldosterone and plasma renin activity were, respectively, smaller and greater. From these results, it appears that during ANGII blockade the sensitivity of ACTH to CRF stimulation is unaffected, whereas that of the adrenals to ACTH is selectively reduced at the level of the zona glomerulosa.
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PMID:Effects of angiotensin II blockade on the responses of the pituitary-adrenal axis to corticotropin-releasing factor in humans. 248 58


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