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)

Exciting developments in knowledge of primary aldosteronism include description of new subtypes and elucidation of the genetic basis of one variety. Furthermore, relatively simple biochemical screening (aldosterone/renin ratio) has disclosed that primary aldosteronism is more common than previously thought, by diagnosing patients at an earlier, normokalaemic stage. The mutant gene discovered in the glucocorticoid-suppressible variety (FHI) codes for an aldosterone biosynythetic enzyme normally controlled by angiotensin II, and now controlled by corticotropin. The zona fasciculata is hyperplastic and makes aldosterone and "hybrid steroids" 18-oxocortisol and 18-hydroxycortisol in excess, in response to ACTH but not to angiotensin II. Adrenal tumours have not yet been described in this condition. Aldosterone-producing adenomas (Conn's syndrome) are also commonly composed of zona fasciculata-like cells, make "hybrid steroids" in excess and are very sensitive to ACTH but not to angiotensin II. We have described a new variety of aldosterone-producing adenoma which is responsive to angiotensin II (AII-responsive APA), consists of at least 20% zona glomerulosa-like cells, and does not make "hybrid steroids" in excess. We have also described a new familial variety of primary aldosteronism that includes tumours and is not glucocorticoid-suppressible (FHII). We propose that primary aldosteronism is a spectrum of genetic diseases expressed as either hyperplasia or neoplasia, and that morphological and genetic diversity explains biochemical and clinical behaviour.
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PMID:Primary aldosteronism: hypertension with a genetic basis. 135 75

Effects of the histamine H1- or H2-receptor antagonists mepyramine (Mep) and cimetidine (Cim) on neuroendocrine and cardiovascular responses to 50 degrees head-up tilt were evaluated in seven human males. Central hypovolemia was characterized by two phases. The first is a normotensive phase with increases in heart rate (HR), total peripheral resistance (TPR), and decrease in cardiac output. Plasma adrenocorticotropic hormone, beta-endorphin, cortisol, catecholamines, and renin activity increased moderately. Normotension lasted 39 +/- 7 min during infusion of saline but was reduced by Mep [18 +/- 3 min, F(2,12) = 9.60, P less than 0.01] and was unaffected by Cim (44 +/- 4 min). The second is a hypotensive phase associated with presyncopal symptoms (hypovolemic shock) and decreases in HR and TPR and a further increase in pituitary-adrenal and sympathoadrenal activity. Decreases in mean arterial pressure and TPR were augmented by Mep, which inhibited release of norepinephrine. Cim inhibited epinephrine release without affecting the development of hypovolemic shock. It is concluded that histaminergic mechanisms are involved in activation of the sympathoadrenal system but not in the pituitary-adrenal axis during central hypovolemia in humans.
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PMID:Pituitary-adrenal responses to head-up tilt in humans: effect of H1- and H2-receptor blockade. 135 10

Sodium nitroprusside was infused intravenously for 10 minutes in normal men, reclining at 45 degrees, in a dose sufficient to decrease the arterial pressure by 10 mmHg. The effect on a variety of plasma hormones was measured during the infusion and for 20 minutes afterwards. The heart rate increased to a maximum of 149%. Norepinephrine rose to a maximum of 196% in 5 minutes. Epinephrine reached a peak of 207% after 10 minutes. Plasma renin activity reached a peak of 449% at 10 minutes. Aldosterone did not change during the infusion, but increased to a maximum of 145% 10 minutes later. Vasopressin increased sharply at the end of the infusion to 893% and then rapidly decreased. Corticotropin, prolactin and growth hormone started to increase toward the end of the infusion, but reached their maxima during recovery. Corticotropin (225%) and prolactin (288%) peaked 10 minutes after the infusion, while growth hormone (414%) appeared still to be rising 20 minutes after the end of the infusion. Cortisol also rose progressively during recovery to a level of 138%. No significant changes were seen in the concentrations of insulin, glucagon, atrial natriuretic peptide, bombesin or neurotensin.
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PMID:Temporal relations of the endocrine response to hypotension with sodium nitroprusside. 155 71

In a double-blind crossover study of 10 normal healthy subjects, we examined the effects of slow-release nifedipine (nifedipine-SR, 10 mg b.i.d) administration on exercise capacity, hormone levels during exercise, and quality of life (QOL) after a 2-week treatment. Two exercise tests, a progressive exercise test and a constant work-rate exercise test, were performed. Maximal oxygen uptake (VO2max) and blood lactate concentration were measured during the progressive exercise test and the exercise intensity corresponding to half lactate threshold (LT), LT, and 4 mmol/l of lactate concentration was determined. Subjects underwent 20 minutes of constant work-rate exercise at each work load, and blood lactate, plasma epinephrine, plasma norepinephrine, plasma renin activity, plasma aldosterone, atrial natriuretic peptide, plasma beta-endorphin, and met-enkephalin were measured. Taking nifedipine-SR had no effect on the responses of blood pressure, heart rate, VO2max, maximal work load, and LT compared to taking placebo. Blood lactate, plasma catecholamine, plasma renin activity, aldosterone, atrial natriuretic peptide, and beta-endorphin levels increased during exercise, and there was no difference between nifedipine-SR and placebo. Met-enkephalin did not increase with either treatment. In the QOL questionnaires, no differences were noted between the two treatments. These findings suggest nifedipine-SR to be a potentially useful drug in view of the lack of effect on exercise capacity, hormone release, and QOL.
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PMID:Administration of slow-release nifedipine does not affect lactate threshold, hormone release during exercise, and quality of life in normal subjects. 157 99

The gonadal axis is thought to modulate adrenocorticotropic hormone (ACTH), arginine vasopressin (AVP), and plasma renin activity (PRA) responses to stimuli in several species. These experiments were designed to compare the responses to hypotension in chronically ovariectomized ewes and intact ewes. The ewes were infused with nitroprusside at rates of 5, 10, or 15 micrograms.kg-1.min-1 or infused with vehicle for 10 min. The response to 15 micrograms.kg-1.min-1 was also tested with or without treatment with 10 mg of dexamethasone 2 h before nitroprusside. Blood samples were collected before and at 5, 10, 15, 20, and 30 min after the start of the infusion for measurement of plasma ACTH, AVP, and PRA. In both groups of animals there were significant responses to hypotension. There was a significant effect of ovariectomy on ACTH, AVP, and PRA responses. ACTH and PRA responses were lower in the ovariectomized ewes; AVP responses were increased in the ovariectomized ewes. Administration of dexamethasone inhibited ACTH responses and did not inhibit PRA responses in both groups of ewes. Administration of dexamethasone did not inhibit the AVP response in the intact ewes but did reduce the response in the ovariectomized ewes.
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PMID:Effect of ovariectomy on vasopressin, ACTH, and renin activity responses to hypotension. 165 Jan 46

The hypothesis that prostaglandin E2 (PGE2) is a circulating mediator of adrenocorticotropic hormone (ACTH) secretion in sheep was tested in conscious adult ewes using 30-min carotid artery infusions of 0, 5, 10, 100, and 500 ng.kg-1. min-1 PGE2 in saline. ACTH, cortisol, and aldosterone were significantly increased during the 500 ng.kg-1.min-1 infusion (166 +/- 61 to 233 +/- 38 pg/ml, 27 +/- 5 to 45 +/- 2 ng/ml, and 52 +/- 11 to 85 +/- 25 pg/ml, respectively). PGE2 infusions of 100 ng.kg-1.min-1 increased ACTH from 104 +/- 31 to 168 +/- 31 pg/ml and cortisol from 18 +/- 5 to 42 +/- 2 ng/ml. PGE2 infusions did not increase arginine vasopressin, plasma renin activity, or hematocrit. Heart rate and mean arterial pressure were minimally but significantly increased during the 500 ng.kg-1.min-1 infusion, from 84.9 +/- 2.8 to 99.3 +/- 5.4 beats/min and 95.5 +/- 1.8 to 101.0 +/- 3.4 mmHg, respectively. In a second study to test whether lower infusion rates of PGE2 increase plasma ACTH in sheep with lower resting hormone concentrations, sheep were infused and sampled through a tether system, preventing any disturbances due to human contact the day of an experiment. For all infusion rates ACTH baselines were less than or equal to 55 +/- 17 pg/ml, and cortisol baselines were less than or equal to 6 +/- 3 ng/ml.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Does intracarotid PGE2 increase plasma ACTH concentration in conscious adult ewes? 165 27

To identify the dynamic response of hormones after burns with special reference to ANP during shock and the subsequent period, plasma concentrations of atrial natriuretic peptide (ANP), aldosterone, cortisol, arginine vasopressin (AVP), corticotropin, (ACTH), plasma renin activities (PRA), norepinephrine (NE) and epinephrine (E) were measured from the day of ICU admission and for 7 days following burn injury. Plasma AVP levels were highest on ICU admission and correlated with size of the burn injury ranged from 20-60 percent of the total body surface area. Between the 5th and 6th postburn day plasma ANP levels elevated while plasma AVP levels returned to normal. Urine sodium concentrations decreased from the 3rd day. Plasma aldosterone levels declined after the 2nd day. Mean epinephrine (E) and norepinephrine (NE) levels elevated on admission and remained elevated throughout the study. These results suggest that ANP plays important role for restoring fluid homeostasis by improving edema in burned tissues during refilling periods in burns.
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PMID:The endocrine response after burns. 165 90

This paper documents an unexpected rise in plasma aldosterone concentration (PAC) to the furosemide-upright test despite a decrease in adrenocorticotropin (ACTH) by dexamethasone, and an unresponsiveness in plasma renin activity to this stimulus in a patient with aldosterone producing adenoma. Furthermore, this patient showed an appropriate response in PAC to a rapid ACTH test, and an insensitivity in PAC to angiotensin-II (Ang-II) infusion. Other factor(s) besides ACTH or Ang-II may play a role in the plasma aldosterone response to ambulation after intravenous furosemide administration in patients with primary aldosteronism.
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PMID:An unexpected rise in plasma aldosterone to furosemide-upright test in primary aldosteronism due to aldosterone producing adenoma. 166 49

Late-gestation fetal sheep respond to slow hemorrhage with increases in plasma concentrations of adrenocorticotropic hormone (ACTH), hydrocortisone, arginine vasopressin (AVP), and plasma renin activity (PRA) that correlate to the acidemia and hypercapnia also produced by hemorrhage. This study was designed to investigate the role of peripheral chemoreceptors in the mediation of these responses. Chronically catheterized fetal sheep were left intact or were subjected to bilateral section of cervical vagosympathetic trunks and carotid sinus nerves. At least 5 days after surgical preparation (between 121 and 138 days of gestation) fetuses were bled at a rate of 11 ml/10 min for 2 h. Denervated fetuses were studied with or without simultaneous infusion of phenylephrine. Denervation exaggerated the decrease in mean arterial pressure and arterial pH and the increase in arterial PCO2 during hemorrhage. Infusion of phenylephrine in the denervated fetuses prevented the decrease in blood pressure and reduced the magnitudes of changes in blood gases. Fetal plasma ACTH, hydrocortisone, and PRA responses to the hemorrhage were exaggerated in the denervated fetuses (not infused with phenylephrine) compared with the intact fetuses. Phenylephrine infusion attenuated the ACTH response and inhibited the AVP response but did not alter the PRA response. We conclude that the sectioned fibers are important for the maintenance of blood pressure and blood gases during hemorrhage and that the PRA, AVP, and ACTH responses to slow hemorrhage are not mediated by peripheral chemoreceptors.
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PMID:Reflex control of fetal arterial pressure and hormonal responses to slow hemorrhage. 173 13

1. Subcutaneous (s.c.) administration of compound 48/80 elicited the increases of water intake, plasma beta-endorphin-like immunoreactivity, hypothalamic 3-methoxy-4-hydroxyphenylethyleneglycol sulfate and Hct in the rats. 2. The s.c. pretreatment of naloxone reduced the compound 48/80-induced water intake but had no effects on other variables. 3. Intracerebroventricular (i.c.v.) injection of naloxone attenuated the compound 48/80- and i.c.v. injected angiotensin II (ANG II)-induced water intake. 4. The hypothalamic norepinephrine metabolism was increased by s.c. injection of compound 48/80 but not by i.c.v. ANG II. 5. The present data suggest the possible involvement of opioid peptide (beta-endorphin) on the compound 48/80- and ANG II-induced thirst. However, it is uncertain whether hypothalamic norepinephrine is involved in the hypovolemic thirst mediated via stimulation of renin-angiotensin system.
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PMID:Participation of opioid peptide (beta-endorphin) and norepinephrine in the control of compound 48/80-induced hypovolemic thirst in the rats. 176 Nov 87


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