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)

A number of mineralocorticoids have been proposed as etiologic factors in low-renin hypertension. In this study, urinary free 19-nor-deoxycorticosterone (UF 19-nor-DOC) was compared to other mineralocorticoids--aldosterone, deoxycorticosterone (DOC), and 18-OH-DOC, in 11 low-renin hypertensive patients on a controlled diet in a metabolic unit. Results demonstrated that both UF 19-nor-DOC and tetrahydro-DOC (TH-DOC) excretion were elevated (2086 +/- 926, nl = 339-579 ng/day, and 18 +/- 7, nl = 5-15 mcg/day, respectively), and positively correlated (r = 0.95). Neither 18-OH-DOC nor aldosterone secretion rates were elevated, and neither of these hormones correlated with UF 19-nor-DOC, with exception of the supine plasma aldosterone (SPA) (r = 0.86). In conclusion, both UF 19-nor-DOC and TH-DOC were increased and positively correlated in the present series of hypertensives. This association is possibly indicative of a precursor-product relationship between DOC and 19-nor-DOC. 19-Nor-DOC, furthermore, correlated with supine plasma aldosterone (SPA), which could, in part, reflect their shared adrenocorticotropic hormone (ACTH) dependence.
Hypertension
PMID:Relationship of 19-nor-deoxycorticosterone to other mineralocorticoids in low-renin hypertension. 634 Dec 21

Stroke-prone, spontaneously hypertensive rats (SP/SHR) were fed a low protein (8%) fish diet + 1% saline at the time of weaning; some were treated with Naloxone (0.4 mg/100 gms bw/sc/2 X daily/5 days per week). Naloxone-treated animals did not develop high blood pressure or strokes. Sixty-two days after feeding the low protein fish diet, blood pressure levels reached 260-300 mmHg and all of the non-treated animals exhibited acute and severe strokes; Naloxone treatment was again initiated for half of the SP/SHR. By Day 4 (post stroke), all of the non-treated SP/SHR were dead; Naloxone-treated SP/SHR survived until Day 12 (post stroke). Naloxone-treatment during the post-stroke period caused significant reduction of blood pressure, ACTH, and beta-endorphin levels concomitant with reduced cerebral edema and clearance of hepatic lipid infiltration. It is suggested that anti-opiate treatment may ameliorate the severe hypertension-inducing effects of a low protein fish diet and thereby prevent the appearance of strokes in SP/SHR as well as palliate the cerebral edema and fatty liver which characteristically appear in the immediate post-stroke period in fish-fed SP/SHR. The central mechanism of this palliative effect may be through reduced hypothalamic-pituitary-adrenal activity.
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PMID:Naloxone ameliorates the pathophysiologic changes which lead to and attend an acute stroke in stroke-prone/SHR. 646 55

An enhanced hypothalamo-pituitary-adrenocortical (HPA) activity has been described during onset of elevated blood pressure in spontaneously hypertensive rats (SHR). An instability of the HPA axis could thus contribute to the development of hypertension in these animals. Glucocorticoid effects on blood pressure and HPA function were studied therefore in SHR and normotensive Wistar-Kyoto (WKY) and Wistar rats. Beginning at 4 weeks of age, the rats were treated with 0.1 and 0.5 microgram betamethasone per milliliter drinking water for 7 weeks. SHR and WKY responded with a significant elevation in average blood pressure. In SHR, mean blood pressure rose from 181.4 +/- 3.9 (mean +/- SEM) to 203.1 +/- 2.8 mm Hg in response to the lower dose of betamethasone and to 209.2 +/- 4.0 mm Hg in response to 0.5 microgram betamethasone per milliliter drinking water. In WKY, blood pressure increased from 134.4 +/- 3.3 to 148.2 +/- 3.0 and 157.9 +/- 4.5 mm Hg in response to the lower and higher dose of betamethasone, respectively. No significant effect was seen in Wistar rats, where the mean blood pressure values changed insignificantly from 133.8 +/- 2.1 to 136.3 +/- 3.2 and 135.6 +/- 2.4 mm Hg. Stress-induced secretion of corticosterone was significantly suppressed in a dose-dependent manner in all three strains. Stress-induced secretion of adrenocorticotropin was markedly reduced by 0.5 microgram betamethasone per milliliter in SHR and by both doses in WKY. No significant effect, however, was seen in Wistar rats. A predisposition to the hypertensiogenic actions of glucocorticoids was found therefore in SHR and WKY, but not in Wistar rats.
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PMID:Long-term effects of betamethasone on blood pressure and hypothalamo-pituitary-adrenocortical function in spontaneously hypertensive and normotensive rats. 664 25

A 39-year-old man with an ACTH producing oncocytic carcinoid of the thymus is reported here. His symptoms were pigmentation, facial and pretibial edema, and high blood pressure. Endocrinological examination revealed the ectopic ACTH syndrome and, especially, high content in the intrathoracic venous blood. On histological examination, the tumor was found to be composed of uniform eosinophilic cells, with no argentaffin granules being demonstrated. Ultrastructural findings revealed a large number of mitochondria and numerous distinct electron-dense neurosecretory granules in the cytoplasm. Abnormally high levels of ACTH, beta-endorphin and gamma-MSH were also found in this tumor tissue. By total extirpation of the tumor, clinical symptoms and laboratory data were entirely normalized.
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PMID:An ectopic, ACTH producing, oncocytic carcinoid tumor of the thymus: report of a case. 674 52

A rare functional black adenoma (FBA) of the adrenal cortex was found to be the cause of hypertension and cushingold features in a 34-yr-old white female. Preoperative studies included [131I]iodocholesterol scanning (ICS) of the adrenal glands, which demonstrated the increased release of cortisol from the affected adrenal gland, with the failure of the opposite adrenal gland to record. This is evidence that cortisol was suppressing adrenocorticotropin (ACTH) output by the pituitary gland. This case documents the clinical utility of "functional" imaging techniques in this clinical setting.
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PMID:[131I]iodocholesterol scintiscan and a rare "functional" black adenoma of the adrenal cortex. 685

Proopiomelanocortin (POMC) is a protein that contains the amino acid sequences of numerous peptide hormones, including the melanocyte-stimulating hormones (MSH). MSH peptides of alpha, beta, and gamma primary structure are present in plasma, and all exhibit natriuretic activity. Intravenous infusion of alpha or beta-MSH leads to a time- and dose-dependent natriuresis, whereas gamma-MSH is reported to be natriuretic at low doses but antinatriuretic at high doses. The natriuretic activity of MSH peptides occurs without change in arterial pressure or renal hemodynamics, suggesting a possible direct tubular inhibition of sodium reabsorption. Intravenously infused gamma-MSH is associated with an increase in the plasma concentration of atrial natriuretic peptide. In addition, gamma-MSH also has a direct intrarenal natriuretic action that is dependent on the renal nerves. In rats, gamma-MSH-related peptides are involved in the reflex control of sodium excretion in situations such as the natriuresis that occurs (a) from the remaining kidney after acute unilateral nephrectomy, (b) from the contralateral kidney shortly after unilateral ureteral pressure elevation, and (c) after unilateral carotid artery traction. POMC-derived peptides (including MSH) are modulated in response to salt loading, and alterations in POMC metabolism and plasma peptide concentrations have been observed in genetically hypertensive rats and during the development of adrenal regeneration hypertension. In addition, plasma gamma-MSH levels are elevated in patients with severe congestive heart failure, and in primary hyperaldosteronism. These observations suggest a possible involvement of MSH-related peptides in sodium homeostasis as well as in certain forms of hypertension.
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PMID:Natriuretic properties of melanocyte-stimulating hormones. 750 15

Increased arterial blood pressure following a pyrogenic reaction has been reported in previous studies, however the mechanism of this hypertension has not been examined in detail. The present study investigated the effects of both intravenous (IV) and intracerebroventricular (ICV) injection of lipopolysaccharide (LPS) from E. coli on body temperature (Tb), mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), calculated total peripheral resistance (CTPR), stroke volume (SV) and plasma levels of adrenocorticotropin (ACTH) and arginine vasopressin (AVP) in conscious, chronically instrumented sheep. IV injection of LPS (1 microgram) increased Tb in a biphasic manner from 38.7 +/- 0.1 to 39.5 +/- 0.2 degrees C after 50 min and to 39.9 +/- 0.2 degrees C after 130 min, and MAP increased biphasically from 64 +/- 1 to 70 +/- 4 mmHg after 40 min and to 78 +/- 3 mmHg after 130 min. CO initially decreased from 4.4 +/- 0.1 to 3.5 +/- 0.1 after 40 min followed by a secondary rise to 4.8 +/- 0.1 l/min after 100 min. This occurred together with a large, biphasic increase in CTPR from 14.5 +/- 1.0 to 22.0 +/- 2.0 mmHg/l/min at 40 min, and to 18.1 +/- 0.1 mmHg/l/min at 120 min. HR increased from 68 +/- 4 to 97 +/- 4 b/min and SV decreased from 65 +/- 2 to 41 +/- 4 ml/beat during the first phase of activation. Plasma ACTH increased from 22 +/- 9 to 1043 +/- 175 pg/ml after 80 min, and plasma AVP increased from 0.7 +/- 0.2 to 12 +/- 4.0 pg/ml after 60 min. ICV injection of LPS produced a long-lasting increase in Tb and MAP, but had no effect on HR or plasma AVP. Plasma ACTH increased from 30 +/- 12 to 427 +/- 110 pg/ml. These changes suggest that intravenous pyrogenic infection produces a potent vasoconstrictor action in sheep to increase blood pressure, possibly mediated by the actions of AVP within the CNS, or other pyrogenically released vasoconstrictor factors. Furthermore, the duration of activation of the cardiovascular system following peripheral and central LPS administration is different, which together with the contrasting effects on ACTH and AVP, indicate the involvement of several hypertensive mechanisms.
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PMID:Pyrogenic stimulation of vascular resistance in conscious sheep. 762 27

We studied the cardiovascular responses to 5 days' infusion of aldosterone (10 micrograms/h) and cortisol (5 mg/h) to determine the possible contribution of mineralocorticoid and glucocorticoid actions to the regional hemodynamic changes caused by corticotropin. These infusion rates produce plasma levels similar to those seen during corticotropin stimulation. In five conscious sheep aldosterone progressively increased mean arterial pressure (P < .001) to a maximum of 11 mm Hg on day 5, whereas cortisol increased pressure by 5 mm Hg (P < .01) within 24 hours. Cardiac outputs on the control day and on day 5 of infusion were 4.4 +/- 0.3 and 4.9 +/- 0.3 L/min, respectively, for aldosterone and 4.3 +/- 0.4 and 5.0 +/- 0.4 L/min for cortisol. Neither steroid significantly altered total peripheral conductance, but they had different, nonuniform regional hemodynamic effects. Mesenteric conductance fell progressively with aldosterone from 7.14 +/- 0.35 (mL/min)/mm Hg to a minimum of 6.17 +/- 0.38 (P < .01) on day 5 of infusion. Mesenteric conductance was transiently reduced with cortisol, but this was not significant over the 5 days. Renal conductance was unchanged with aldosterone, but cortisol caused a rapid, sustained increase in renal conductance from 2.9 +/- 0.3 to 4.0 +/- 0.4 (mL/min) / mm Hg (P < .001) within 24 hours, similar to the increase caused by corticotropin. As with corticotropin there were only minor changes in the coronary and iliac vascular beds. In summary, these two endogenous steroids had contrasting, nonuniform regional hemodynamic effects, aldosterone causing mesenteric vasoconstriction, and cortisol causing renal vasodilatation.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1995 Aug
PMID:Regional hemodynamic and endocrine effects of aldosterone and cortisol in conscious sheep. Comparison with the effects of corticotropin. 763 38

This case report describes a 68-year-old man with Cushing's syndrome due to adrenocorticotropic hormone (ACTH)-independent bilateral adrenocortical macronodular hyperplasia (AIMAH). He was referred to our hospital for evaluation of bilateral enlargement of the adrenal glands found incidentally by computed tomography (CT). He had a ten-year history of hypertension. Although he was normokalemic and did not show Cushingoid features, the diagnosis of ACTH-independent Cushing's syndrome was established by endocrinological examinations. His plasma cortisol showed no diurnal rhythm and was unsuppressible by high-dose (8 mg/day) dexamethasone. Plasma ACTH was undetectable and did not respond to corticotropin-releasing hormone. Excised adrenal glands were markedly enlarged (right 28 g and left 64 g). Macroscopic appearance of the glands showed multiple yellowish nodules typical for AIMAH; microscopic findings were also compatible with AIMAH. The present case indicates that patients with AIMAH sometimes do not show typical Cushingoid features and therefore AIMAH can be found incidentally from ultrasound or CT examination of the abdomen.
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PMID:Non-cushingoid Cushing's syndrome due to adrenocorticotropic hormone-independent bilateral adrenocortical macronodular hyperplasia. 764 19

Exposure to lead has been postulated to contribute to elevated blood pressure in humans and has been shown to raise blood pressure in animals. The mechanism of action of lead on blood pressure is unknown. We fed lead to rats in their drinking water and then examined the production of aldosterone by their adrenal cells in vitro. We also measured excretion of aldosterone and corticosterone by intact rats stimulated with corticotropin, with and without lead treatment. At a dose (273 ppm) that raised blood levels to 30 to 40 micrograms/dL, comparable to blood levels in exposed humans, lead induced increased aldosterone secretion in vitro and in vivo. The effect of lead was most evident when cells or animals were stimulated with aldosterone secretagogues. Experiments in vitro indicate that exposure to lead in vivo increases activity of one or more steps in the late pathway of aldosterone biosynthesis. The results suggest that the hypertensive effect of lead involves relative hyperaldosteronism and may be most evident when secretion of this hormone is stimulated.
Hypertension 1995 Apr
PMID:Lead increases aldosterone production by rat adrenal cells. 772 33


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