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)

The control of aldosterone secretion may be altered during acute changes in arterial blood gases. We studied the blood gas, plasma electrolyte, renin (PRA), adrenocorticotropic hormone (ACTH), and aldosterone (ALDO) responses to acute hypercapnia (4 and 8% CO2), acute hypocapnic hypoxia (10% O2), acute severe normocapnic hypoxia (7% O2-4% CO2), and acute hypercapnic hypoxia (7% O2-8% CO2) in conscious, cannulated Long-Evans rats. Normoxia resulted in normal levels of PRA (6.9 +/- 2.0 ng.ml-1.h-1), ACTH (96 +/- 32 pg/ml), and ALDO (10 +/- 3 ng/dl). Hypercapnia had no effect on PRA but did lead to an increase in ACTH (to 298 +/- 69 pg/ml) and ALDO (to 33 +/- 7 ng/dl) during 8% CO2 exposure. Normocapnic hypoxia resulted in a significant increase in ACTH (to 196 +/- 14 pg/ml) and ALDO (to 30 +/- 3 ng/dl). Hypercapnic hypoxia resulted in the greatest increases in PRA (to 30 +/- 2 ng.ml-1.h-1), ACTH (to 397 +/- 114 pg/ml), and ALDO (to 41 +/- 5 ng/dl). We conclude that in conscious rats 1) hypercapnia (less than 80 Torr) had no significant effect on PRA, 2) isocapnic, severe hypoxia (Po2 approximately 34 Torr) increased ACTH, and 3) the combination of hypercapnia and hypoxia was a very potent stimulus to PRA, ACTH, and ALDO. The ALDO responses to increases in endogenous ACTH and angiotensin II appear to be normal in conscious rats during acute hypoxia and/or hypercapnia.
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PMID:Renin, ACTH, and aldosterone during acute hypercapnia and hypoxia in conscious rats. 283 42

The responses of adrenocorticotropin (ACTH), renin, epinephrine and norepinephrine and arterial pressure and heart rate (HR) to hypotensive hemorrhage were examined before and 1 h after lesion of the paraventricular nuclei (PVN) in pentobarbital-anesthetized rats and 1 day before and 4 days after lesion of the PVN in conscious rats. The ACTH response to hemorrhage was abolished 1 h (n = 8) and 4 days (n = 14) after PVN lesion whereas the ACTH response in the sham groups (in both anesthetized and conscious studies, n = 8 and 16 respectively) remained intact. PVN lesion had no effect on basal ACTH levels 4 days after lesion. The responses of renin, epinephrine, norepinephrine and mean arterial blood pressure (MABP) and HR to hemorrhage were not affected 1 h or 4 days after PVN lesion. Resting levels of the above variables did not change 4 days after lesion. The PVN lesion had a small (but significant) effect on the baroreceptor reflex in the conscious study (reflex changes in HR caused by phenylephrine- or nitroglycerin-induced change in MABP) and had no effect on the baroreceptor reflex in the anesthetized study. The group with PVN lesions gained more weight 6 days after lesion than the group with sham lesions. We conclude that the PVN are part of a neural pathway involved in ACTH regulation during perturbations of the cardiovascular system and on weight gain and that PVN lesions have little or no effect on resting or stimulated (hemorrhage) levels of renin, epinephrine, norepinephrine, HR and MABP or on the baroreceptor reflex.
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PMID:Paraventricular lesions: hormonal and cardiovascular responses to hemorrhage. 283 86

The effects of ovine corticotropin releasing factor (o-CRF) on plasma aldosterone, 18-OH-corticosterone (18-OHB), plasma adrenocorticotropin (ACTH) and cortisol were determined in eight patients with primary aldosteronism, six with aldosterone-producing adenoma (APA) and two with idiopathic hyperaldosteronism (IHA). The results were compared with those in six normal subjects and eleven patients with essential hypertension (EHT, 5 with low renin and 6 with normal renin). In patients with APA, the peak plasma aldosterone and 18-OHB responses to 100 micrograms iv of o-CRF (226% and 113% increase from baseline, respectively) were greater than those in EHT and normal subjects. The net integrated aldosterone and 18-OHB responses (840 +/- 156, and 419 +/- 121 ng/dl.hr, respectively) were also significantly greater (p less than 0.01) in APA than those in normals and EHT. In two patients with IHA, both the peak and net integrated aldosterone response were smaller than those in APA, in spite of nearly identical plasma ACTH and cortisol responses. These results suggest that augmented responses of mineralocorticoids to o-CRF may be characteristic of aldosteronism due to APA, mediated by CRF-induced ACTH, and possibly other proopiomelanocortin (POMC)-derived peptides.
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PMID:Effects of corticotropin-releasing factor (CRF) on aldosterone and 18-hydroxycorticosterone in essential hypertension and primary aldosteronism. 283 82

Previous studies from this laboratory have demonstrated that intravenous infusions of hydrocortisone (cortisol) into fetal sheep at rates that produce plasma concentrations achieved during fetal stress inhibit fetal adrenocorticotropic hormone (ACTH) and renin secretion. The present study was designed to test for inhibition of fetal renin and ACTH after maternal adrenal secretion of cortisol. ACTH-(1-24) or saline infusion into 12 pregnant ewes (120-132 days gestation) at rates of 0, 1, 5, or 20 ng ACTH.kg-1.min-1 for 5 h produced dose-related increases in maternal plasma ACTH and cortisol concentrations and fetal plasma cortisol concentration. In the 20-ng.kg-1.min-1 group, increases in fetal plasma cortisol of 8.0 ng/ml (to 24.3 +/- 3.7 ng/ml) did not suppress basal fetal plasma renin activity. One hour after the end of the maternal vehicle or ACTH infusion, fetal ACTH secretion was stimulated by fetal intravenous infusion of sodium nitroprusside. In the 0-, 1-, and 5-ng.kg-1.min-1 groups, fetal ACTH responses to nitroprusside were suppressed in animals infused with ACTH. Together, these results indicate that the maternal adrenal secretion of cortisol inhibits stimulated secretion of ACTH but not renin in 120- to 132-day-gestation fetal sheep.
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PMID:Are fetal adrenocorticotropic hormone and renin secretion suppressed by maternal cortisol secretion? 284 58

1. Physical effort involves, along with an increase in the plasma concentration of beta-endorphin, profound adaptations of the circulation and the endocrine system. The effects of opioid antagonism on the responses of blood pressure, heart rate and several hormones to exercise were therefore studied in 10 normal men. They exercised in the supine position up to 33% and 66% of their maximal exercise capacity and received in a randomized double-blind cross-over protocol, either saline or naloxone (10 mg intravenously, followed by a continuous infusion of 10 mg/h). 2. Intra-arterial pressure and heart rate were continuously monitored, but were not affected by naloxone. 3. At rest, opioid antagonism produced a rise in plasma renin activity and in plasma adrenocorticotropin, cortisol and aldosterone, but only the stimulation of the two adrenocortical hormones differed significantly from the control experiments; at rest naloxone also prevented the fall in plasma adrenaline, which occurred with saline infusion. Furthermore, the exercise-induced rises in plasma angiotensin II, aldosterone, cortisol, noradrenaline and adrenaline were higher on naloxone than on saline, while a similar tendency was also present for the increases with exercise in plasma renin activity and plasma adrenocorticotropin. Neither at rest nor during exercise did opioid antagonism alter plasma lactate and glucose and serum insulin and growth hormone. 4. In conclusion, (1) endogenous opioids are not involved in the responses of blood pressure and heart rate to supine exercise; (2) at rest and during exercise, the endogenous opioids inhibit the secretion of adrenocorticotropin, aldosterone, cortisol, noradrenaline and adrenaline; (3) they also inhibit the plasma renin-angiotensin II system indirectly via the catecholamines.
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PMID:Effects of opioid antagonism on the haemodynamic and hormonal responses to exercise. 284 14

Arginine vasopressin may play a role in the control of adrenocorticotropic hormone release during stress in the adult animal. Arginine vasopressin is also considered an important stress hormone in the fetus. The effect of arginine vasopressin infusion on adrenocorticotropic hormone release in the fetus was investigated in 14 chronically cannulated ovine fetuses with normal blood gas and pH values between 103 and 137 days' gestation. There was a significant increase in adrenocorticotropic hormone and cortisol levels during a 30-minute infusion of arginine vasopressin. Plasma renin activity was unchanged. The corticotropin-releasing activity of arginine vasopressin was not blocked by pretreatment with a V1-receptor antagonist and was not significantly different when the pressor response was attenuated by sodium nitroprusside infusion.
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PMID:Arginine vasopressin infusion stimulates adrenocorticotropic hormone and cortisol release in the ovine fetus. 284 87

A tilt-table test was performed on 12 untrained subjects to evaluate the humoral adaptation to postural change. The observed peripheral reaction with a reversible short-term rise of norepinephrine (NE) and plasma renin activity (PRA) allowed us to divide the syndrome of the orthostatic dysregulation into a hyponoradrenergic and hypernoradrenergic type. This classification can be helpful for the clinical evaluation and therapy of orthostatic lability. The central excessive stimulation of the antidiuretic (ADH) and adrenocorticotropic hormone (ACTH) follow-ing orthostatic symptoms such as weakness or dizziness was not completely reversible within the observation period of 30 min. The ADH and ACTH increase was not different between the hypo- and the hypernoradrenergic type of dysregulation but was the most sensitive indicator of orthostatic lability: 41% of all subjects showed a hypernoradrenergic orthostatic dysregulation with pronounced NE response and alpha 2-adrenoceptor down-regulation. By use of antiembolism stockings (AES) or dihydroergotamine (DHE) this rate decreased to 16%. This was associated with a significantly reduced NE and PRA response and a diminished alpha 2-adrenoceptor number.
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PMID:Humoral regulation of the orthostatic reaction. 284 55

The present study evaluated a protocol for drawing large volumes of blood over an acute time frame in conscious cannulated rats with blood from cannulated donor rats simultaneously infused to maintain isovolemia. During time control (n = 6), three successive 1.5-ml blood samples were drawn at 10-min intervals with equal volumes of donor blood infused simultaneously. One milliliter of blood was drawn quickly and saved for analysis followed by an additional 3 ml of blood withdrawal to total a 15-ml/kg hemorrhage. Two subsequent 1.5-ml samples were replaced with autologous (hemorrhage) blood. During hypoxia inspired O2 was decreased to 10% after the first sample-transfusion. The sampling-transfusion protocol (time control) had no effect on blood pressure (MAP), hematocrit (Hct), blood gases, renin, or adrenocorticotropic hormone (ACTH). Hemorrhage resulted in a significant decrease in MAP, Hct, base excess, and arterial PCO2 and an increase in arterial PO2, renin activity, and ACTH. Ten percent O2 resulted in significant hypoxemia, respiratory alkalosis, and a small degree of hypotension at the 20-min sample with no change in renin and a moderate increase in ACTH. The consistency of the results with previous studies confirms the utility and efficiency of large sample-transfusion protocols for the study of blood gas and endocrine dynamics in conscious rats.
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PMID:Evaluation of a blood sample-transfusion protocol in rats: blood gases, renin, and ACTH. 284 65

The results of investigation of the secretion of hypophyseal, adrenal and renal hormones resulting from parlodel administration in 44 patients with Itsenko-Cushing disease were discussed. Concentrations of corticotropin (ACTH), prolactin, somatotropin (STH), thyrotropin (TSH), cortisol, aldosterone, adrenalin, noradrenaline, dopamine and blood renin activity were determined by radioimmunoassays and radioenzymatic methods on an empty stomach and 30, 60 min., 2, 4 and 24 h after parlodel administration (2.5 mg) per os. Parlodel administration in Itsenko-Cushing disease was shown to cause a decrease in the secretion of hypophyseal hormones (ACTH, prolactin and STH). The level of cortisol raised before the start of the investigation was gradually decreased after the drug administration and reached its minimum in 2-4 h. Correlation of the basal level of aldosterone and blood renin activity, and a response of the renin-angiotensin-aldosterone system to parlodel administration was revealed. Changes in the secretion of catecholamines were of diverse nature: a decrease in the blood concentration of noradrenaline in the absence of adrenalin and dopamine shifts.
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PMID:[Effect of a single dose of parlodel on the secretion of various hormones in Itsenko-Cushing disease]. 285 Nov 39

The purpose of this study was to define the temporal relationship between anterior pituitary hormone profiles and rapid-eye-movement (REM) sleep occurrence. Plasma levels of prolactin (PRL), adrenocorticotropic hormone (ACTH), luteotropin (LH), thyroid-stimulating hormone (TSH) and growth hormone (GH) were measured in 10 min blood samples. Analysis of the nocturnal profiles for these hormones and the concomitant patterns of sleep stage distribution indicate that the onset of REM sleep very seldom occurred during the increasing phase of secretory episodes. In 93-98% of cases, depending on the hormone studied, it occurred either during the declining phase, at peak level, or at nadir, each of these phases reflecting a decrease in glandular activity. This relationship differed from the very close association previously found between the sleep stage alternation and plasma renin activity. These findings seem to fit in with the concept of reduced sympathetic activity and disruption of the vegetative functions during REM sleep.
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PMID:REM sleep in humans begins during decreased secretory activity of the anterior pituitary. 285 40


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