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 effect of synthetic melanocyte-stimulating hormones (MSH) on urinary excretion of sodiu, potassium and water was studied in hamsters. Synthetic alpha-MSH and synthetic human beta-MSH showed a marked natriuretic and diuretic effect depending on the dosage of hormone. The natriuretic effect of both hormones was approximately equal and did not parallel the magnitude of the melanocyte-stimulating activity of the investigated peptides. Both peptides showed also a milder kaliuretic effect independent on their dose. The rise of the sodium/potassium index in urine was significant after both peptides. Bilateral adrenalectomy increased further the natriuresis induced by alpha-MSH, while it did not affect the effect o MSH on diuresis and kaliuresis. Changes in urinary excretion of sodium and potassium are considered to be consequence of direct renal action of MSH.
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PMID:Natriuretic and kaliuretic effect of melanocyte-stimulating hormones in hamsters. 31 65

Evidence for the existence of a hormone that is stimulable by adrenocorticotropic hormone (ACTH) and capable of causing hypertension has been collected in several patients. This hormone is not a known mineralocorticoid or glucocorticoid. The hypothesis that a steroid can produce hypertension was tested in an 18-year-old man with dexamethasone-suppressible hypertension. During dexamethasone treatment, when aldosterone secretion was suppressed, less than normal and the patient was normotensive, steroids were given by constant infusion in an attempt to reproduce the hypertension of the dexamethasone-free state. Hypertension was not caused by 5 days of administration of aldosterone, 18-hydroxydeoxycorticosterone (18-OH-DOC) at 1 mg/day, or deoxycorticosterone (DOC) at 30 mg/day. However, sodium retention and potassium loss were observed during infusion of aldosterone and DOC. Hypertension was produced within 5 days during infusion of ACTH or oral metyrapone. The hypertensive effect of the metyrapone was eliminated by the additional treatment with aminoglutethimide. These studies suggest that an ACTH-dependent steroid rather than aldosterone, 18-OH-DOC, or DOC may be the cause of the hypertension in this patient. Study of a 3-year-old child who presented with short stature, hypertension, hypokalemic alkalosis, suppressed renin and ACTH, and decreased excretion of all known steroids suggested excessive secretion of a pressor hormone. Reversal of the hypertension and hypokalemic alkalosis occurred when spironolactone was administered. ACTH exacerbated the clinical and biochemical abnormalities, suggesting that the secretion of the unknown factor was dependent on ACTH. A study of the urinary steroids revealed remarkably low excretion of aldosterone and cortisol. Plasma levels of ACTH were low. The low production of aldosterone was not associated with the increased excretion of precursor metabolites. These finding suggest the secretion of an unknown hypertensive factor of remarkably high potency, with the ability to suppress the secretion of both renin and ACTH.
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PMID:Mineralocorticoid hypertension in childhood. 32 86

Aldosterone excretion (AE) and plasma renin activity (PRA) were measured in eight untrained (UT) and eight endurance-trained (TR) male subjects before and during 4 h head-out immersion to study the mechanism of reduced renal sodium excretion in athletes. AE was significantly lower before immersion, and decreased less during immersion, in TR than in UT. Fractional sodium excretion, too, was lower and increased less during immersion in TR than in UT. PRA decreased in the water bath in all subjects (p less than 0.001) with no significant difference between the groups. During immersion, plasma sodium concentration oscillated whereas potassium concentration showed a temporary rise in TR (p less than 0.001). The attenuated response of AE in TR may be due partly to this increase of plasma potassium concentration. The generally reduced aldosterone release in TR might be caused by a training induced adaptation of the adrenals to corticotropin. The lowered renal sodium excretion of TR in spite of the decreased AE suggests an intensified aldosterone effect in these subjects, diminishing the salt loss during exercise.
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PMID:Reduced aldosterone and sodium excretion in endurance-trained athletes before and during immersion. 39 64

The rate of release of beta-endorphin-like immunoreactivity (beta-EI) from rat hypothalamic slices was increased 3- to 4-fold over the spontaneous release during exposure to a depolarizing concentration of potassium ions. This augmented outflow was abolished in the absence of calcium. The amount of beta-EI released from slices exposed to a second pulse of potassium was reduced by approximately 50% compared to that in the first. 70% of the potassium-induced released immunoreactive material migrated on a calibrated Sephadex G-50 column like synthetic human beta-endorphin. These findings are discussed in terms of a neuronal release of beta-endorphin and may be taken as supportive evidence for a neurotransmitter and/or neurohormonal role of beta-endorphin in the hypothalamus.
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PMID:Release of beta-endorphin from rat hypothalamus in vitro. 46 98

The rate of release of beta-endorphin immunoreactivity from the anterior lobe of the rat pituitary in vitro increased in respone to potassium-induced depolarization in a calcium-dependent manner. Potassium-induced depolarization did not, however, change the rate of release from intermediate/posterior lobe. These findings provide support for the view that beta-endorphin may have a humoral function and suggest that beta-endorphin stores in discrete pituitary areas are regulated by different release mechanisms.
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PMID:Release of beta-endorphin from rat pituitary in vitro. 69 83

Responses of plasma renin activity, plasma aldosterone, plasma cortisol, and plasma electrolyte concentration and urinary electrolyte and aldosterone excretion were studied in four men during hypoxic decompression to a stimulated altitude of 4,760 m in a pressure chamber. Three of the four subjects developed significant acute mountain sickness. Plasma sodium and potassium concentrations were unchanged. No significant change in plasma renin activity was observed, but values tended to fall. Plasma aldosterone concentration was depressed while plasma cortisol was elevated and diurnal variation lost. Urinary sodium excretion was unchanged, but urinary potassium and aldosterone excretion were decreased. The decrease in plasma and urinary aldosterone and urinary potassium in the absence of change in plasma renin activity or plasma potassium is of uncertain origin. It is unlikely to be due to a decrease in adrenocorticotropin secretion since plasma cortisol rose during the same time. None of the changes could be causally implicated in the development of acute mountain sickness although the increase in plasma cortisol was greatest in the most ill.
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PMID:Renin, aldosterone, electrolyte, and cortisol responses to hypoxic decompression. 91 12

Endothelin-1 (ET-1) binds to specific receptors in cultured bovine adrenal glomerulosa cells and stimulates aldosterone secretion with a 50% effective concentration (EC50) of 300 +/- 80 pM (mean +/- SE). The relative stimulatory potency for ET-1 is significantly less than that of angiotensin II (ANG II). The incubation of calf zona glomerulosa cells in primary culture with ET-1 and ANG II resulted in a significant potentiation of ANG II effect on aldosterone secretion. The EC50 of ET-1 potentiation of ANG II-induced stimulation of aldosterone secretion was 40 +/- 5 pM (mean +/- SE, n = 4), which is lower than the EC50 for ET-1 stimulation of aldosterone secretion. Adrenocorticotropic hormone (ACTH) stimulation of aldosterone secretion, but not that of potassium, was also potentiated by ET-1, but to a lesser degree. ET-1 and ET-1-mediated potentiation of ANG II-stimulated aldosterone biosynthesis increased both the early and late pathways of aldosterone biosynthesis, but the potentiation was greater for the early pathway. Preincubation with ET-1 for at least 15 min, followed by extensive washing to remove bound ET-1, also resulted in persistent potentiation of ANG II-mediated aldosterone secretion. ET-2, sarafotoxin, and vasoactive intestinal contractor potentiation of ANG II action were very similar to that of ET-1. ET-3 and Big-ET-1 potentiated ANG II stimulation only at the highest doses tested and the proendothelin-(110-130) fragment was inactive. ET-1 potentiation of ANG II action is likely to be mediated through an ETB receptor subtype.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endothelin-1 potentiation of angiotensin II stimulation of aldosterone production. 131 Feb 39

To assess the effect of extracellular hydrogen ion concentration (PH+) on aldosterone secretion, studies in which other known modulators could be controlled were performed on 13 patients undergoing hemodialysis. High (35 mM) or low (14-17 mM) dialysate bicarbonate concentrations were utilized on separate days to either decrease or increase PH+, while plasma potassium concentrations (PK) were held at constant levels and changes in plasma renin activity (PRA) were minimized by avoiding changes in body weight. Changes in PH+ were associated with concordant changes in plasma aldosterone concentration (Pa) in both high- and low-bicarbonate studies. When these changes in Pa in high- and low-bicarbonate studies were analyzed together as a function of corresponding changes in PH+, a significant correlation could be demonstrated (r = 0.659, P less than 0.001). There was no correlation between changes in Pa and changes in PK, plasma sodium, plasma adrenocorticotropic hormone (ACTH), or PRA. Using the same methods to control PH+ and other variables during hemodialysis, the effects of altered PH+ on ACTH-stimulated aldosterone and cortisol secretion were evaluated in studies on six patients who received incremental infusions of ACTH after pretreatment with dexamethasone. In these studies, there was no demonstrable effect of PH+ on Pa or plasma cortisol concentration. We conclude that physiological changes in PH+ have a weak modulating effect on basal aldosterone secretion that may not be evident in the presence of other acutely applied stimuli.
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PMID:Modulation of plasma aldosterone by physiological changes in hydrogen ion concentration. 131 33

Angiotensin II (Ang II) inhibits renin secretion and production from the kidney, but the effect of Ang II on adrenal renin is not clear. Nephrectomy, via elevated plasma adrenocorticotropic hormone (ACTH) and potassium, is a strong stimulator of adrenal renin production in the rat. This stimulation is inhibited by the infusion of Ang II, suggesting a negative feedback between Ang II and adrenal renin. In the present study, we examined the effect of Ang II on adrenal renin using a primary culture of rat glomerulosa cells. Cells were exposed to ACTH (10(-11) M), high potassium (8 and 12 mM), db-cyclic AMP (db-cAMP), (10(-3) M), or Ang II (10(-11) to 10(-5) M) for 24 hours, and active renin and inactive renin were measured. Active renin was predominant in the cells, whereas inactive renin predominated in the medium. Ang II stimulated renin production in a dose-dependent fashion (cell-active renin, 1.21 +/- 0.20 to 2.39 +/- 0.16; medium-inactive renin, 2.59 +/- 0.40 to 6.14 +/- 0.49 ng Ang I/10(6) cells). Both ACTH and db-cAMP significantly stimulated active renin in the cells (ACTH, 1.73 +/- 0.14 to 9.44 +/- 0.98; db-cAMP, 1.45 +/- 0.16 to 3.96 +/- 0.71 ng Ang I/10(6) cells) and inactive renin in the medium (ACTH, 4.98 +/- 0.38 to 43.7 +/- 5.63; db-cAMP, 3.80 +/- 0.32 to 33.55 +/- 5.62 ng Ang I/10(6) cells). The addition of Ang II (10(-7) M) blunted the stimulation of renin production by both ACTH and db-cAMP by 60%. High potassium-stimulated renin production was not inhibited by Ang II.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of angiotensin II on renin production by rat adrenal glomerulosa cells in culture. 131 12

An inhibitory effect on water, sodium and potassium excretion occurs after both systemic and central injections of morphine, beta-endorphin and other opioid peptides. Some investigators claimed that antidiuretic hormone release could be a mechanism explaining opioid-induced oliguria. Injection into the subfornical organ of a synthetic Met-enkephalin analog (FK 33824) reduced urine outflow as well as renal Na+ and K+ excretion. Identical effects were observed in hypophysectomized or in median eminence-lesioned rats. In addition, no changes were seen in blood pressure after FK 33824 injection into the subfornical organ. These results suggest that opioid stimulation of this structure induces an inhibitory effect on renal water, Na+ and K+ excretion, and that antidiuretic hormone release is probably not important to these phenomena.
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PMID:Role of opioid peptides and subfornical organ in the renal function of intact and hypophysectomized rats. 131 88


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