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)

To investigate possible abnormalities of the hypothalamic-pituitary axis in patients with chronic renal failure on dialysis, we have examined the effects of insulin-induced hypoglycemia on the adrenal steroid responses. In normal subjects, plasma aldosterone and cortisol concentrations increase significantly in response to hypoglycemia, with good correlation. In the patients with end-stage renal disease (ESRD) however, insulin-induced hypoglycemia fails to elicit significant increases in the plasma cortisol and aldosterone levels. To test the adrenal responsiveness to adrenocorticotropin (ACTH), we administered ACTH to both groups. Plasma cortisol and aldosterone responses are similar in both groups suggesting that the adrenal responsiveness to ACTH is not impaired. We also investigated the responsiveness of the renin-angiotensin-aldosterone system in response to volume contraction by hemofiltration in patients with ESRD. Neither plasma renin activity nor plasma aldosterone concentration change significantly following such contrived volume contraction. These results reveal several endocrinologic abnormalities in the patients with ESRD on chronic hemodialysis.
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PMID:Aldosterone response to insulin-induced hypoglycemia in hemodialysis patients. 254 16

Adrenocorticotropic hormone (ACTH), arginine vasopressin (AVP), and renin responses to hemorrhage are highly correlated to the hemorrhage-induced decreases in arterial pH. The present study was designed to test the responses of these three systems to acute fetal acidemia, produced by intravenous infusion of H+. HCl was infused into chronically catheterized fetal sheep at rates of 0.02 (n = 5), 0.10 (n = 6), and 0.50 (n = 5) meq/min. Infusions at rates of 0.10 and 0.50 meq/min significantly decreased fetal arterial pH and increased arterial PCO2. Fetal heart rate and plasma concentrations of ACTH, cortisol, and AVP were significantly increased during infusion of HCl at 0.5 meq/min. Neither fetal plasma renin activity nor fetal arterial blood pressure was significantly altered by any of the infusions. The results of these experiments suggest that fetal ACTH, AVP, and heart rate are stimulated by decreases in arterial pH and/or increases in arterial PCO2. We speculate that these responses are chemoreceptor mediated, although we cannot distinguish the apparent relative roles of peripheral and central chemoreceptors on the basis of the present study.
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PMID:Acidemia stimulates ACTH, vasopressin, and heart rate responses in fetal sheep. 254 8

Serotonergic stimulation can increase the secretion of several hormones through the involvement of different serotonin (5-HT) receptor subtypes. RU 24969, a 5-HT agonist with highest affinity at 5-HT1A and 5-HT1B receptors, increased plasma renin activity (PRA) and plasma renin concentration (PRC) as well as plasma corticosterone and prolactin concentrations in a dose-dependent manner. Inasmuch as 5-HT2 receptors mediate the serotonergic stimulation of renin secretion, we examined the ability of two selective 5-HT2 antagonists, ritanserin and LY53857, to inhibit the neuroendocrine effects of RU 24969. To determine whether the 5-HT receptors which are involved in the stimulation of these hormones are pre- or postsynaptic, RU 24969 was also injected to rats whose brain serotonergic neurons were chemically destroyed by i.c.v. injection of 5,7-dihydroxytryptamine. Both ritanserin and LY53857 blocked the effect of RU 24969 on PRA and PRC, but did not inhibit the RU 24969-induced elevation in plasma corticosterone concentrations. Ritanserin did not inhibit the effect of RU 24969 on prolactin levels, but LY53857 produced a partial inhibition of the RU 24969-induced elevation of prolactin concentrations. In rats with chemical lesions of serotonergic neurons the dose-response curves of RU 24969 for PRA and PRC as well as corticotropin, corticosterone and prolactin shifted to the left, suggesting functional up-regulation of postsynaptic 5-HT receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neuroendocrine evidence for denervation supersensitivity of serotonin receptors: effects of the 5-HT agonist RU 24969 on corticotropin, corticosterone, prolactin and renin secretion. 255 18

An effect of enalapril maleate on the activity of renin-angiotensin-aldosterone system and sympathetic reactivity, erythrocyte prostaglandin and sodium levels as well as blood beta-endorphin was investigated in 28 patients with the essential arterial blood hypertension. It was found that enalapril maleate significantly increased plasma renin activity, decreased plasma norepinephrine and its 24-hour excretion, and decreased erythrocyte beta-endorphin and sodium levels. Blood epinephrine and aldosterone levels and their daily excretion remained unchanged similarly to prostaglandins. The above results suggest that a decrease in sympathetic system activity and intracellular sodium concentration may play a role in the hypotensive action of enalapril maleate related to the inhibition of angiotensin II formation.
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PMID:[Effect of treatment with enalapril maleate on the levels of circulating catecholamines, beta endorphins, prostaglandins, and concentration of sodium in erythrocytes in patients with essential hypertension]. 255 61

To evaluate to what extent opioid secretion in exercise induces the release of atrial natriuretic factor (ANF), six healthy male volunteers who were trained subjects, were submitted to two maximal exercise tests with and without (control) opioid receptor blockade by Naltrexone. Blood samples were drawn before (rest) and after exercise (post-exercise) in order to measure human ANF (alpha h ANF), beta-endorphin, plasma aldosterone concentration (PAC) plasma renin activity (PRA) and adreno-cortico trophic hormone (ATCH) by radio-immunological methods. Expired gas was collected during exercise to measure oxygen consumption. On average, the same maximal oxygen consumption (VO2max) during exercise was reached by all subjects with and without treatment. Plasma ANF level at rest slightly decreased after administration of Naltrexone; the response to physical exercise was significantly reduced by Naltrexone. There was no statistical difference between plasma levels of beta-endorphin, PRA and ACTH at rest nor in the post-exercise situation under the influence of Naltrexone. The PAC increased significantly at rest after Naltrexone administration but there was no statistical difference between both values after exercise. These data demonstrate that: (1) ANF secretion during exercise is influenced by the level of beta-endorphin in the plasma; (2) the possible inhibitory role of ANF on aldosterone secretion during exercise is probably over-ruled by the increase in plasma ACTH and PRA.
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PMID:Influence of endogenous opioids on atrial natriuretic factor release during exercise in man. 255 88

It was been shown that physical exercise increases plasma atrial natriuretic peptide (ANP) level. This effect was attributed to the hemodynamic changes of exercise which could increase atrial volume and result in ANP secretion. On the other hand, it was evidenced that morphine and opiate peptides greatly stimulate ANP release. To evaluate to what extent the endogenous opioid secretion during exercise induces the ANP release, six healthy volunteers male trained subjects were submitted to two maximal exercise tests with and without (placebo) opiate receptors blockade by naltrexone (50 mg per os). Blood samples were drawn before (rest) and after maximal exercise in order to measure by radioimmunological methods human atrial natriuretic peptide (alpha-h-ANP), beta-endorphin, plasma aldosterone (ALD), plasma renin activity (PRA) and corticotrophin (ACTH). Expired gas was collected during exercise to measure oxygen consumption. Subjects reached the same value of maximal oxygen consumption (VO2 max) at the end of exercise whatever treatment. Plasma ANP level at rest decreases slightly after administration of naltrexone (32.8 +/- 6.3 pg/ml with placebo versus 21.3 +/- 4.6 pg/ml with naltrexone) but the response to physical exercise was significantly reduced by naltrexone (73.3 +/- 14.9 pg/ml with placebo versus 46.9 +/- 8.6 pg/ml with naltrexone) (p less than 0.05). There was no statistical difference according to the treatment between the plasma levels of beta-endorphin, PRA and ACTH at rest as well as at the end of a maximal exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Atrial natriuretic peptide response to physical exercise is inhibited by an antagonist of the opioid receptors]. 256 Oct 15

Hypotension in fetal sheep stimulates reflex decreases in heart rate and increases in the secretion of several hormones, including adrenocorticotropin (ACTH), cortisol, vasopressin, and renin. However, little is known about the afferent limb(s) of the reflex(es) controlling these responses. Fetal sheep between 122 and 134 days gestation were prepared with chronic vascular catheters, intravascular balloon-tipped catheters, and amniotic fluid catheters. Seven fetal sheep were also subjected to sinoaortic denervation, and nine remained intact. After recovery from surgery for 2-5 days, fetuses were subjected to a 10-min period of hypotension produced by vena caval obstruction, produced by inflation of balloons in the superior and inferior venae cavae. Vena caval obstruction produced decreases in fetal heart rate and increases in fetal plasma ACTH, vasopressin, and renin activity, which were related to the degree of hypotension. Prior sinoaortic denervation attenuated all of these responses. It is concluded that afferent fibers in the carotid sinus and/or aortic depressor nerves mediate part of the heart rate, ACTH, vasopressin, and renin responses to vena caval obstruction in late-gestation fetal sheep.
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PMID:Sinoaortic denervation attenuates the reflex responses to hypotension in fetal sheep. 271 52

Experiments were designed to evaluate the central and systemic effects by enkephalins and the enkephalin analogue FK-33824 on mean arterial pressure (MAP) and heart rate (HR) in conscious sheep. Intracerebroventricular infusion of FK-33824 increased both MAP and HR in a dose-dependent manner in normal sheep. The increases in MAP and HR were attenuated by naloxone administered centrally, but not systemically. Intracerebroventricular infusion of met-enkephalin, leu-enkephalin and naloxone failed to change both MAP and HR significantly. However, intravenous infusion of met-enkephalin, leu-enkephalin and FK-33824 resulted in bradycardia. Haemorrhage alone decreased both MAP and HR. Intracerebroventricular infusion of FK-33824 blunted the reduction in MAP in response to haemorrhage. The increases in MAP and HR following FK-33824 were also accompanied by elevated levels of plasma renin concentration. It is suggested that the tachycardia and pressor effect produced by the intracerebroventricular administration of FK-33824 in normal conscious sheep may result from a combined action of both neural and chemical pathways which are involved in cardiovascular control, and are mediated via the mu-opioid receptors. Opioids may have opposite effects on cardiovascular control depending on the route of administration.
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PMID:Effects of enkephalins and the analogue FK-33824 on mean arterial pressure and heart rate in conscious sheep. 274 83

The role of angiotensin II in the hormonal and renal responses to maximal exercise was investigated by using the angiotensin-converting enzyme inhibitor captopril. Nine male subjects performed a standardized maximal treadmill test with and without acute captopril treatment (25 mg orally). At rest, captopril elevated plasma renin activity and lowered aldosterone levels. With maximal exercise, captopril treatment reduced the increase in mean arterial blood pressure by 8 mmHg and the increase in plasma renin activity by 3.0 ng ANG I.ml-1.h-1. The responses of adrenocorticotropin (ACTH), cortisol, and vasopressin to maximal exercise were not altered by captopril treatment. Although aldosterone levels were reduced at rest with captopril, during maximal exercise no difference was noted between treatments. Captopril treatment had no effects on the renal handling of salts or water during exercise. In conclusion, angiotensin II plays a role in the increase in mean blood pressure during maximal exercise in normal subjects but has no effect on the exercise responses of ACTH, vasopressin, and aldosterone or on the renal handling of salts and water.
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PMID:Hormonal and renal responses to converting enzyme inhibition during maximal exercise. 282 83

The activity of plasma renin, concentration of serum aldosterone and plasma corticotropin were determined by a radioimmunoassay in 78 patients with diffuse toxic goiter with thyrotoxicosis of various degrees of gravity, im 21 patients with primary hypothyroidism and 25 controls in euthyroid condition. In the patients with thyrotoxicosis such investigations were conducted before and after a course of drug therapy. In thyrotoxicosis the activity of the renin-angiotensin-aldosterone system was raised, in hypothyroidism it was lowered, a degree of expression of appropriate changes being associated with the gravity of disease. In the patients with marked thyrotoxicosis after a course of drug therapy the indices of plasma renin activity and serum aldosterone concentration did not return to normal. Hypophyseal corticotropic function was raised in marked thyrotoxicosis, mild hypothyroidism and corresponded to the normal level in the patients with hypothyroidism of average gravity. Plasma ACTH concentration in the patients with marked thyrotoxicosis returned to normal after a course of drug therapy.
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PMID:[State of the renin-angiotensin-aldosterone system in thyroid pathology based on the results of radioimmunoassay]. 283 33


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