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)

In normal adult rats anesthetized with urethane, intravenous injections of beta-endorphin (30--150 micrograms kg-1) induced a transient fall of blood pressure followed by a small hypertension and a prolonged hypotension. Prior administration of naloxone completely blocked these effects, whereas naloxone, given 1 hr after beta-endorphin, did not reverse the prolonged depressor phase of the opioid peptide. The effects of beta-endorphin on the arterial blood pressure were greatly reduced in animals pretreated with p-chlorophenylalanine, a specific depletor of serotonin. Moreover, in rats pretreated with potent serotonin antagonists such as cyproheptadine, mianserin, and metergoline, beta-endorphin did not produce a significant hypotension. Furthermore, the depressor effect of beta-endorphin was potentiated by fluoxetine, a specific serotonin uptake inhibitor. These observations suggest the participation of a serotonergic pathway in the action of beta-endorphin on the arterial blood pressure.
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PMID:Systemic administration of beta-endorphin: potent hypotensive effect involving a serotonergic pathway. 15 30

Plasma 16 beta-hydroxydehydroepiandrosterone (16 beta-OH-DHEA) levels were measured by radioimmunoassay in normal and pathological conditions in man. 16 beta-OH-DHEA levels in normal subjects rose sharply during adolescence and then declined slowly throughout adult life: 192 pg/ml age 7-11, 395 pg/ml age 15-19, 330 pg/ml age 20-39, 261 pg/ml age 40-59, and 124 pg/ml over 60-years-old. No marked difference was seen between male and female subjects. 16 beta OH-DHEA rose significantly (p less than .01) during adrenocorticotropin (ACTH) stimulation, declined (p less than .005) during dexamethasome suppression and during gonadal suppression, rose (p less than .05) during gonadal stimulation and following administration of WIN 24540, an inhibitor of 3 beta-o1-dehydrogenase (p less than .005). 16 beta-OH-DHEA levels in adrenal venous blood were higher than in inferior vena cava blood but the levels in hepatic venous blood were not higher than in arterial blood. These results indicate that 16 beta-OH-DHEA is secreted directly by the adrenal cortex and probably the gonads. 16 beta-OH-DHEA levels were elevated in normal pregnant women, pregnant women with toxemia and in patients with Cushing's disease, ectopic ACTH-producing tumor and congenital adrenal hyperplasia but not in patients with low-renin essential hypertension.
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PMID:Plasma 16 beta-hydroxydehydroepiandrosterone in normal and pathological conditions in man. 18 75

A 53-year-old male with Cushing's syndrome due to ectopic ACTH production from medullary carcinoma of the thyroid was reported. The clinical course and results of detailed endocrinological studies and immunohistochemical findings about the cancer tissue were described. An abnormally high concentration of calcitonin, ACTH and beta-MSH in both plasma and cancer tissue (thyroid, lymph nodes and liver) were documented by radioimmunoassay. Urinary 17-OHCS was as high as 38.4 mg/day and showed no supression following dexamethasone 8 mg/day administration. ORAL METYRAPONE (3 G/DAY) CAUSED NO RESPONSE IN URINARY 17-OHCS. Parallel increments in plasma calcitonin, ACTH and beta-MSH were observed following calcium and gastrin loading. Total thyroidectomy with modified radical neck dissection caused minimal changes of plasma levels of calcitonin, ACTH and beta-MSH and no improvement in the clinical manifestations of Cushing's syndrome. An aortogram revealed metastatic tumors in the liver. A second operation, total adrenalectomy, resulted in an improvement of the clinical and laboratory findings such as hypokalemia, high blood pressure, muscle atrophy and moon face. Immunofluorescent study showed different distribution patterns in calcitonin- and ACTH-positive cells in the primary focus but similar patterns in the liver metastasis.
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PMID:[A case of medullary thyroid carcinoma with ectopic ACTH syndrome (author's transl)]. 20 14

Male and female, nonarteriosclerotic (virgin) and arteriosclerotic (breeder), Sprague-Dawley rats were subjected to the hypertension-producing regimen of uninephrectomy, 1% saline drinking water, and desoxycorticosterone (Percorten) pivalate. Just before autopsy, some of the animals were given a single injection of corticotropin. The acute challenge of corticotropin caused a definite increase in free fatty acids, systolic blood pressure, creatine phosphokinase, glucose, and corticosterone. The two weeks of desoxycorticosterone and 1% saline-induced hypertension caused myocarditis and hyalinization of the coronary arteries of the nonarteriosclerotic (virgin) rats and definite exacerbation of the preexisting arteriosclerosis in breeder rats, severe myocarditis, and polyarteritis nodosa. All of the treated animals manifested lipid depletion of the zona glomerulosa indicative of reduced biosynthesis and secretion of endogenous mineralocorticoids due to the exogenous desoxycorticosterone and saline treatment.
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PMID:Corticotropin stimulation of hypertensive rats with and without arteriosclerosis. 21 53

1. Administration of adrenocorticotropic hormone (ACTH) to sheep produced increases in mean arterial pressure within 24 h associated with an increase in cardiac output and cardiac rate. Both cardiac output and blood pressure remained elevated over the 5 days of ACTH treatment. 2. Administration of ACTH during beta-adrenoreceptor blockade resulted in an increase in blood pressure without changes in cardiac output at 24 h. 3. Administration of a combined steroid infusion over 5 days produced increases in cardiac output identical with the effects of ACTH but with a substantially smaller effect on blood pressure. 4. These data suggest that the observed changes in cardiac output produced by ACTH treatment may be associated with high blood concentrations of adrenocortical steroids rather than being necessary for the development of the hypertension.
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PMID:Haemodynamics of ACTH-induced hypertension in sheep. 23 25

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

Eighteen patients treated with prednisone on alternate days for varying degrees of alopecia areata (AA) were examined a mean of 15 months after discontinuation of the drug. Despite an initial response to the therapy, long-term benefit was not thought to be substantial. Numerous side effects related either to systemic corticosteroids or to AA were apparent during the course of therapy, as well as at the time of the evaluation reported herein. Acne, obesity, lenticular opacities, mild hypertension, and impaired adrenocorticotropic hormone (ACTH) reserve were among the findings noted. Long-term treatment was not accompanied by an obvious beneficial change in the natural course of AA. Because of the potentially serious side effects and the lack of substantial improvement in the eventual course, alternate-day prednisone therapy is not recommended for long-term use in AA.
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PMID:Prednisone therapy for alopecia areata. A follow-up report. 79 Nov 52

Implantation of a mammotropic tumor (MtTF4), secreting growth hormone, prolactin, and corticotropin, in female rats of Fischer F344 strain causes hypertension, vasculitis, renal and cardiac hypertrophy, and extensive renal and cardiac lesions. When rats of the same strain were implanted with the MtTF4 tumor but sodium was withheld from the diet, systolic blood pressure rose more slowly but by six weeks reached the same values recorded in the animals implanted with the tumor and allowed to consume sodium ad libitum. In the rats, on sodium deficient diet, however, the vascular damage as well as the renal and cardiac lesions were minimal or absent. Implantation of the tumor caused adrenal cortical dysfunction, and elevated levels of deoxycorticosterone were seen in the peripheral plasma of the rats of all three groups. Nonetheless, plasma deoxycorticosterone was significantly lower in rats on a sodium deficient diet as compared with those having sodium added to the diet. Light microscopic and ultrastructural studies of the adrenal glands revealed that the lack of dietary sodium largely prevented the extensive damage of the zona fasciculata cells usually seen in the tumor-bearing rats, consuming sodium ad libitum. Both hypertensive MtT tumor-bearing animals and normotensive controls on a sodium deficient diet had a conspicuous increase of renal content of renin. It is evident that hypertension may be produced in rats bearing the MtTF4 tumor even in the virtual absence of dietary sodium. It does not appear that the hypersecretion of renal renin sustains the hypertension in these rats, since high levels of this substance were seen in the kidney of normotensive controls on the same sodium deficient diet. Elevated levels of plasma DOC may possibly explain the hypertension. In addition, it is likely that the animals may also have elevated levels of glucocorticoids.
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PMID:Deveolpment of hypertension in rats maintained on a sodium deficient diet and bearing a mammotropic tumor (MtTF4). 81 73

A 4-year-old girl had abdominal distention, muscular weakness, renal tubular dysfunction, and hypertension associated with hypokalemic metabolic alkalosis. There were no clinical symptoms of cortisol deficiency, but there was excessive deoxycorticosterone and cortisocsterone production. Basal plasma aldosterone levels were undetectable; however, adrenocorticotropic hormone (ACTH) stimulation brought plasma aldosterone levels up to normal. The urinary pregnanediol, tetrahydro-deoxycorticosterone (THDOC), and tetrahydrocorticosterone (THB) concentrations were elevated. Stimulation of ACTH failed to increase urinary 17-ketosteroid, 17-hydroxycorticosteroid, or plasma cortisol levels significantly, while urinary THDOC, THB, and plasma corticosterone concentrations were further elevated. The elevated plasma corticosteroid intermediates were suppressed by dexamethasone administration. When physiologic doses of dexamethasone were administered, the hypertension, electrolyte imbalance, and abnormal corticosteroid secretion were all corrected. The studies indicated a partial 17alpha-hydroxylase defect in this patient.
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PMID:Hypokalemic crisis simulating intestinal obstruction in a 4-year-old girl. A consequence of 17alpha-hydroxylase deficiency. 97 20

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)
Hypertension 1992 Mar
PMID:Effect of angiotensin II on renin production by rat adrenal glomerulosa cells in culture. 131 12


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