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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors studied the effect of adrenocorticotropic hormone (ACTH), potassium and plasma renin activity on blood aldosterone in normal subjects as well as in patients with essential hypertension (of a labile and stable course) and hyperaldosteronism (primary and idiopathic). It was demonstrated that in normal subjects and patients with labile essential hypertension, the secretion of aldosterone was simultaneously stimulated by the renin-angiotensin system (RAS) and the hypothalamus-adenopituitary. The RAS dominated in normal conditions whereas in labile hypertension the hypothalamus-adenopituitary system was predominant. In stable hypertension, the RAS and hypothalamus-pituitary influenced aldosterone secretion in an equal degree. Hyperaldosteronism was associated with the most pronounced deviations in the relationship between stimulants and aldosterone. In addition to decreased plasma levels of renin activity and potassium, the corticotropic activity of the hypothalamus-adenopituitary was increased during the first 10 years of the disease, while later on the function of this system became inhibited. The highest ACTH levels were recorded in idiopathic hyperaldosteronism.
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PMID:[Concentration of adrenocorticotrophic hormone and aldosterone secretion in essential hypertension and hyperaldosteronism]. 298 49

This study evaluates dopaminergic regulation of aldosterone secretion in 6 patients with high spinal cord transections. Administration of the dopamine antagonist metoclopramide resulted in a marked rise in plasma aldosterone and 18-hydroxycorticosterone levels in 12 normal individuals, but no change in plasma levels of these zona glomerulosa corticosteroid products in spinal cord patients. Spinal cord transected patients also did not have the rise in plasma renin activity that was observed in normals following metoclopramide administration. Basal levels of aldosterone, 18 hydroxycorticosterone, corticosterone and renin activity as well as the aldosterone responses to graded dose infusion of adrenocorticotropin were similar in the spinal cord patients and the normals. These data suggest that dopaminergic regulation of adrenal zona glomerulosa corticosteroid and renal renin secretion is absent in patients with high spinal cord transections, suggesting that intact neural pathways from the central nervous system are necessary for metoclopramide stimulation of aldosterone and renin secretion in men. Since basal plasma aldosterone levels were normal in spinal cord transected patients, it appears that the absence of dopaminergic control does not result in elevated secretion.
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PMID:Absent aldosterone response to metoclopramide in patients with high spinal cord transection: evidence that metoclopramide stimulates aldosterone secretion through central pathways. 298 37

The effects of halothane anaesthesia or epidural analgesia on the per- and postoperative change in blood concentrations of ACTH, beta-lipotropin, cortisol, dehydroepiandrosterone, aldosterone, glucose, lactate and free fatty acids were investigated in connection with elective orthopaedic surgery. Anaesthesia in man with halothane and nitrous oxide was found to be associated with a significant increase in plasma ACTH levels and beta-LPH levels. Changes in plasma dehydroepiandrosterone were similar to those in plasma cortisol. The elevation of plasma aldosterone during major surgery could be explained as the effect of an increased renin secretion. However, simultaneous increase in plasma cortisol and plasma aldosterone during surgery reflect an additional effect of adrenocorticotropin upon aldosterone secretion.
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PMID:[Behavior of the hypophyseal-adrenal cortex system in inhalation and conduction anesthesia. A review with comparative study]. 299 12

This study examines the effects of the synthetic atrial peptides (atriopeptin I, II, and III) on aldosterone and corticosterone production by rat adrenal cell suspensions. Furthermore, we studied the effect of atriopeptin II infusion on the plasma aldosterone response to angiotensin II in the rat in vivo. Atriopeptin I, II, and III decreased aldosterone release from zona glomerulosa cells in a dose-dependent fashion. 10 pM atriopeptin II inhibited basal aldosterone release significantly (P less than 0.01), and 10 nM atriopeptin II or III lowered it by 79%. Atriopeptin II decreased the sensitivity of the glomerulosa cells to adrenocorticotropic hormone (ACTH) and angiotensin II. Atriopeptin II had no effect on basal or ACTH-stimulated corticosterone release by fasciculata-medullary cells. In vivo infusions of angiotensin II with or without simultaneous infusions of atriopeptin II showed that atriopeptin II significantly inhibited the aldosterone response to angiotensin II. This inhibition by atriopeptin II was independent of any effect on plasma renin activity, serum potassium, or ACTH. These data raise the possibility that the atrial natriuretic peptides may affect sodium excretion by the kidney, not only directly, but also indirectly through the inhibition of aldosterone production.
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PMID:Effect of atrial peptides on aldosterone production. 299 88

This study examined the plasma aldosterone and corticosteroid responses to a 60-min infusion of adrenocorticotropin (ACTH) or angiotensin (ANG) II started immediately after an acute isotonic saline volume expansion (0.5 ml . kg-1 . min-1 for 30 min). Five conscious dogs of either sex with exteriorized carotid loops were used in this repeated-design study. Volume expansion per se caused a 10% decrease in hematocrit, a 12.5% decrease in plasma protein, and a 2.7-mmHg increase in central venous pressure with no change in mean arterial pressure, heart rate, or plasma sodium. Volume expansion per se also resulted in significant reductions in vasopressin, plasma renin activity, ACTH, aldosterone, and corticosteroid levels. The aldosterone responses to ACTH and ANG II were significantly inhibited (46-71%) by acute volume expansion. The corticosteroid response to ACTH was 19-29% inhibited by volume expansion. We conclude that acute volume expansion significantly inhibits the adrenocortical sensitivity to its tropic hormones probably via alterations of synergistic factors.
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PMID:Acute volume expansion decreases adrenocortical sensitivity to ACTH and angiotensin II. 299 12

To assess the role of endogenous opioids in the secretion of pituitary and adrenal hormones, we injected intravenously the antagonist naloxone (1 mg/kg) into six dogs, euhydrated or dehydrated. Plasma renin activity (PRA), osmolality, and concentrations of adrenocorticotropic hormone (ACTH), cortisol, aldosterone, vasopressin, Na+, and K+ were measured. Dehydration elevated (P less than 0.05) PRA, vasopressin, osmolality, and Na+. Thirty minutes after injection of naloxone, osmolality, Na+, K+, hematocrit, and plasma protein were not altered. Naloxone-induced elevations of ACTH (25 +/- 10 and 22 +/- 4 pg/ml) and cortisol (4.8 +/- 1.0 and 5.1 +/- 1.0 micrograms/dl) were similar during euhydration and dehydration, respectively. The increase in aldosterone due to naloxone was greater after euhydration (7.7 +/- 3 ng/dl) than during dehydration (2.3 +/- 0.8 ng/dl). Naloxone increased vasopressin by (5.3 +/- 2.8 microU/ml) during dehydration but not during euhydration. Intravenous hypertonic saline infusions showed that naloxone potentiates the osmotic release of vasopressin. Our results indicated that dehydration did not alter the inhibitory role of opioids in regulation of ACTH and cortisol but suppressed the inhibition of aldosterone secretion. Our findings also showed that opioids inhibit secretion of vasopressin during dehydration by decreased responsiveness to osmotic stimulation.
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PMID:Pituitary and adrenal hormone responses to naloxone in euhydrated and dehydrated dogs. 300 81

We studied the effect of chronic hypoxia on the renin, adrenocorticotropin (ACTH), aldosterone, and corticosterone responses to acute hemorrhage in conscious male rats with chronic femoral arterial catheters. Rats were exposed to 21, 12.5, or 10% O2 (n = 7 per group). At 42 h of exposure, animals underwent a rapid 6 ml/kg hemorrhage. O2 at 12.5 and 10% led to significant hypoxemia (arterial PO2 = 52 +/- 1 and 43 +/- 1 Torr, respectively) and respiratory alkalosis. Significant increases in plasma sodium to 145 +/- 2 meq/l and decreases in plasma potassium to 3.53 +/- 0.12 meq/l were also observed during hypoxia. Hypoxia per se had no significant effect on blood pressure, plasma renin activity, ACTH, and corticosterone. O2 at 12.5% led to a significant reduction in aldosterone levels (0.9 +/- 0.8 ng/dl) compared with normoxia (4.2 +/- 0.9 ng/dl). The mean arterial pressure, plasma renin activity, and aldosterone responses to hemorrhage were unaltered by hypoxia. ACTH and corticosterone responses to hemorrhage were potentiated by exposure to 10% O2. We conclude that chronic exposure to severe hypoxia augments the pituitary-adrenal but not the renin-aldosterone response to hemorrhage.
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PMID:Renin, ACTH, and adrenocortical function during hypoxia and hemorrhage in conscious rats. 300 36

Fetal adrenocorticotropin (ACTH) and renin secretion are increased by a variety of stimuli and decreased by cortisol negative feedback inhibition. However, the time courses of these interactions are unknown. The present studies were designed to test for rapid feedback negative suppression of ACTH and renin secretion in fetal and adult sheep. In chronically catheterized fetal sheep, ACTH and renin secretion were stimulated by intravenous infusion of sodium nitroprusside, a vasodilator drug. Vehicle or cortisol, infused at rates of 1, 2, or 4 micrograms/min for 2 min before and during the infusion of nitroprusside did not significantly alter the fetal ACTH or renin responses to nitroprusside. In five nonpregnant ewes, chronically prepared with skin loops containing the carotid arteries, nitroprusside (20 micrograms X kg-1 X min-1) was infused beginning 2 min after infusion of vehicle or cortisol (3.5 or 7 micrograms X kg-1 X min-1). Cortisol infusion produced a rising plasma cortisol concentration similar to that after stress but did not alter the magnitude of the ACTH response to nitroprusside. The results indicate that cortisol-induced suppression of ACTH secretion does not occur rapidly in the fetal or adult sheep and that the cortisol-induced suppression of fetal plasma renin activity is a slow process.
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PMID:Absence of fast negative feedback control of ACTH and renin in fetal and adult sheep. 300 21

Previous experiments demonstrated that increases in ovine fetal plasma cortisol concentration to maximal stress levels suppressed fetal plasma renin activity and completely inhibited fetal adrenocorticotropin (ACTH) responses to subsequent stress. This study was designed to quantitate the suppressive action of cortisol on both ACTH and renin. Fetal sheep between 117 and 131 days gestation were surgically prepared with chronically implanted catheters. At least 4 days after surgery, vehicle or cortisol (0.25, 0.5, 1, 2, or 3 micrograms/min) were infused for 5 h. One hour after the end of the vehicle or cortisol infusion, fetal ACTH and renin secretion were stimulated by intravenous infusion of sodium nitroprusside. Cortisol infusions suppressed basal plasma renin activity (caused by suppression of plasma renin concentration) to degrees that were related to the increases in fetal plasma cortisol concentration. After cortisol infusions, renin responses to hypotension were apparently suppressed to degrees not obviously related to the rate of cortisol infusion. Fetal plasma ACTH responses to hypotension were completely suppressed by increases in total and unbound fetal plasma cortisol concentration 1.6 and 1.7 ng/ml, respectively. These results demonstrate a high sensitivity of the fetal hypothalamopituitary unit and renin-angiotensin system to cortisol.
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PMID:Sensitivity of cortisol-induced inhibition of ACTH and renin in fetal sheep. 301 Jul 46

This study was designed to investigate adrenocorticotropin (ACTH), cortisol, and renin responses to nitroprusside-induced hypotension in adult sheep. Five sheep were surgically prepared with carotid arterial skin loops at least 1 yr before these experiments. After catheterization of the carotid arteries and external jugular veins the sheep were infused with nitroprusside intravenously at rates of 0, 10, 15, or 20 micrograms . kg-1 . min-1 for 10 min. Nitroprusside produced significantly dose-related decreases in mean arterial pressure and increases in heart rate, plasma ACTH and cortisol concentrations, and plasma renin activity. Hematocrit was significantly increased in the 10- and 20-micrograms . kg-1 . min-1 groups during nitroprusside, probably reflecting contraction of the spleen. After the end of the period of hypotension, hematocrit was significantly decreased in all nitroprusside infusion groups, probably reflecting transcapillary movement of fluid into the vascular space. A posteriori analysis of the data suggests that the ACTH response to nitroprusside infusion was better predicted by the nadir in mean arterial pressure and that the renin activity response was better predicted by the initial rate of decrease of mean arterial pressure during nitroprusside infusion.
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PMID:ACTH, cortisol, and renin responses to arterial hypotension in sheep. 301 9


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