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)

E2078, a new analgesic is a dynorphin derivative. E2078 shows strong affinity to kappa receptors and is not rapidly cleaved by peptidases. This analgesic is also considered to be free of tolerance and dependence. In the present study, to determine the effect of E2078 on pituitary-adrenocortical function the author administered E2078 (0.001, 0.05, 0.1, 1.0, 10.0 mg.kg-1) by intramuscular injection to 38 adult mongrel dogs under enflurane anesthesia (1.0%) and then investigated the changes in the plasma concentrations of ACTH, cortisol, beta-endorphin, PRA, aldosterone and ADH. In the animal groups which received E2078 at dosages of 0.001, 0.05, 0.1, and 1.0 mg.kg-1, no significant differences in the plasma concentrations of each hormone were detected compared with the control group which received physiological saline by intramuscular injection. However, in the dog group which received E2078 at 10.0 mg.kg-1, the plasma concentrations of PRA and aldosterone were significantly elevated.
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PMID:[Effects of E2078, a new dynorphin derivative, on pituitary-adrenocortical functions in dogs]. 197 31

Atrial natriuretic peptide (ANP) has been identified in the central nervous system and its participation in regulation of various regulatory brain functions has been postulated. To elucidate whether central ANP influences endocrine systems related to blood pressure regulation and renal excretory functions, effects of infusion of ANP at a rate of 120 ng.min-1 into the third cerebral ventricle on plasma level of epinephrine (E), norepinephrine (NE), renin, vasopressin and beta-endorphin as well as on excretion of urine, sodium, potassium (UKV) solutes and free water (CH2O) were investigated in conscious dogs. Significant decrease of plasma E from 77.6 +/- 7.0 to 62.1 +/- 4.8 pg.ml-1 and of NE from 345.5 +/- 20.7 to 286.4 +/- 15.0 pg.ml-1 was found at the end of 30 min lasting ANP infusion. Significant elevation of PRA and UKV and a decrease in CH2O were found 60 min after ANP infusion. No significant changes in other variables were found. In time control experiments plasma hormones concentration and renal excretory functions were not significantly influenced. The results suggest that central ANP may affect the sympatho-adrenal outflow.
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PMID:Central effects of atrial natriuretic peptide on plasma catecholamines, vasopressin, renin and beta-endorphin and on renal excretory functions in the dog. 214 67

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

Controversy surrounds the issue of whether beta-endorphin affects adrenal steroidogenesis. Recent work has both supported and refuted the claim that beta-endorphin stimulates a rise in serum aldosterone. We investigated the role of beta-endorphin in adrenal steroidogenesis by examining its potential modulation of the response of serum cortisol to exogenous ACTH (Cosyntropin). Four of five normal men received: 1) synthetic beta-endorphin (1 microgram/kg X min) for 30 min, followed by a bolus dose of 0.2 micrograms ACTH; 2) beta-endorphin (100 micrograms, iv), followed by 0.2 micrograms ACTH iv; 3) 0.2 micrograms ACTH iv; and 4) beta-endorphin (100 micrograms iv) alone. The integrated cortisol response to exogenous ACTH, calculated as the area under the cortisol response curve, was significantly less when the ACTH infusion was preceded by the 30-min beta-endorphin infusion than when administered alone [163 +/- 50 (SE) microgram/dl X min vs. 282 +/- 51 micrograms/dl X min, respectively; P less than 0.01]. By contrast, there was no difference between the integrated cortisol response to exogenous ACTH alone and exogenous ACTH after the bolus dose of beta-endorphin (282 +/- 51 vs. 293 +/- 39 micrograms/dl X min, respectively). Beta-Endorphin (30-min infusion or 100-micrograms bolus dose alone) caused no change in serum aldosterone, dehydroepiandrosterone, or PRA. Serum PRL levels, however, were raised significantly (P less than 0.05) by the 30-min infusion of beta-endorphin. The infusion and bolus doses of beta-endorphin raised plasma beta-endorphin levels to over 100,000 pg/ml and 5,000 pg/ml, respectively. We conclude that very high plasma levels of beta-endorphin may influence the response of cortisol to ACTH through a direct effect on the adrenal cortex. However, even in disease states such as Addison's and Nelson's diseases, such levels of plasma beta-endorphin are not known to be achieved.
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PMID:Beta-endorphin attenuates the serum cortisol response to exogenous adrenocorticotropin. 300 53

An association between increased blood pressure levels and hypoalgesia has been reported in the experimental animal and in man. The relation between pain perception and cardiovascular function is however still obscure. In order to gain some insight into this aspect, normotensive subjects with low and high tolerance to pain, as assessed by tooth pulp stimulation, were compared for blood pressure and heart rate during cold pressor test, 24 hr urinary catecholamines, supine and upright PRA and plasma beta-endorphin levels. No significant difference was observed between the two groups for casual blood pressure, heart rate and PRA. Compared to subjects with low tolerance to pain, those with high tolerance to pain were significantly older and had: 1) significantly higher levels of diastolic blood pressure and of beta endorphin levels during cold pressor test; 2) significantly higher beta-endorphin levels after cold pressor test; 3) a significantly higher excretion of noradrenaline (but not of adrenaline and dopamine).
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PMID:Relationship between pain sensitivity, cardiovascular reactivity to cold pressor test and indexes of activity of the adrenergic and opioid system. 307 26

We studied the effect of chronic carotid body denervation on renin (plasma renin activity, PRA), adrenocorticotropin (ACTH), blood pressure, and hematocrit responses to acute normocapnic (arterial CO2 partial pressure, PaCO2, 35 Torr) and hypercapnic (PaCO2, 65 Torr) hypoxia (arterial O2 partial pressure, PaO2, 31 Torr) in five anesthetized, artificially ventilated dogs. Animals were studied at least 3 days before and again at least 10 days after carotid body denervation (bilateral carotid sinus nerve resection). Increases in PRA during hypercapnic normoxia [21.8 +/- 6.4 ng angiotensin I (ANG I) X ml-1 X 3 h-1] and normocapnic hypoxia (13.3 +/- 4.2 ng ANG I X ml-1 X 3 h-1) were not attenuated by carotid body denervation. Increases in ACTH during normocapnic hypoxia (117 +/- 34 pg/ml) were attenuated but not eliminated by carotid body denervation; the increase in ACTH during hypercapnic hypoxia (295 +/- 93 pg/ml) was not attenuated by carotid body denervation. Both the blood pressure and hematocrit responses to normocapnic and hypercapnic hypoxia were attenuated by carotid body denervation. We concluded that 1) the renin response to hypercapnia and hypoxia is not a carotid chemoreflex, 2) the ACTH response to hypoxia is partially a carotid chemoreflex, and 3) blood pressure and hematocrit responses to hypoxia are primarily carotid chemoreflexes.
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PMID:Renin and ACTH responses to hypercapnia and hypoxia after chronic carotid chemodenervation. 608 93

Hemodynamic stability is better preserved during bicarbonate hemodialysis compared to acetate. We have studied the effects of bicarbonate (HDB) and acetate hemodialysis (HDA) on plasma levels of vasoactive substances. The treatments were performed for 270 min. A cuprophan plate dialyzer was used. The ultrafiltration volume and the ultrafiltration rate were identical in the individual patients during the two treatments. In the case of vasoconstrictors there was an increase in neuropeptide Y (NPY) (20%, p < 0.01) during HDB and arginine vasopressin (AVP) was unchanged. Unlike this was the response during HDA when there was no change in NPY and a decrease in AVP (38%, p < 0.01). An increase in noradrenaline (NA) (41%, p < 0.05) occurred during HDA different from what was the case during HDB. There was a gradual increase in renin (PRA) during both HDB (141%, p < 0.05) and HDA (148%, p < 0.01). With respect to vasodilators there were no differences between the two regimes regarding calcitonin gene-related peptide (CGRP) and motilin (MOT). The change in substance P (SP) during the treatments was also similar but somewhat more pronounced during HDB. Thus, an initial rise occurred (HDB, 81%, p < 0.01; HDA, 36%, p < 0.05) followed by a decrease (HDB, 26%, p < 0.05) or a tendency to decrease (HDA, 12%, p = 0.058) during the remaining part of the treatment. A rise in beta-endorphin (beta-END) occurred during HDB (10%, p < 0.05) but not during HDA. An increase in vasoactive intestinal peptide (VIP) occurred during HDB (27%, p < 0.05) different from the decrease during HDA (11%, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in plasma levels of vasoactive substances during routine acetate and bicarbonate hemodialysis. 800 26

Mean arterial blood pressure (MAP), heart rate (HR) and arterial plasma levels of corticotropin (ACTH), renin activity (PRA) and catechols [norepinephrine (NE), epinephrine (EPI), and the intraneuronal NE metabolite dihydroxyphenylglycol (DHPG)] at baseline and in response to the serotonin-1C/2 (5-HT1C/5-HT2) agonist 1-(2,5-dimethoxy-4-iodophenyl)2-aminopropane (DOI, 1.0 mg/kg i.a.) in conscious, freely-moving, juvenile (4 week old) spontaneously hypertensive rats (SHR's) and age-matched Wistar-Kyoto (WKY) normotensive control rats were measured simultaneously. Baseline levels of MAP, NE, DHPG, and EPI all were significantly higher in the SHR's. There was a similar trend for PRA, but ACTH did not differ between the two strains. DOI produced marked increases in levels of MAP, ACTH, EPI, and also PRA but did not affect NE or DHPG concentrations. HR decreased only in the WKY group after administration of DOI. The magnitudes of the EPI and ACTH responses did not differ between the rat strains. Responses of MAP and PRA were significantly larger in SHR's. These results suggest that there is a selective hyperresponsiveness of PRA and blood pressure to 5-HT2 receptor stimulation parallel to a deficient baroreceptor reflex in juvenile SHR's.
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PMID:Plasma catecholamine, renin activity, and ACTH responses to the serotonin receptor agonist DOI in juvenile spontaneously hypertensive rats. 823 34

Plasma concentrations of beta-endorphin (beta-EP), leucine enkephalin (LEK), arginine vasopressin (AVP), neurotensin (NT), renin activity (PRA) and angiotensin II (AT-II) were determined before and after the treatment with clonidine in 117 patients with essential hypertension. Before the treatment, the patient group had lower levels of beta-EP and LEK (P < 0.001), higher levels of AVP, PRA and AT-II (P < 0.05-0.01), as compared with those in control group. After 14 days of the treatment, plasma levels of beta-EP, LEK increased significantly (P < 0.001), and correlated negatively with the decrease of the mean artery pressure (r = -0.369 and r = -0.441, respectively, P < 0.01). PRA and AT-II decreased significantly (P < 0.05, P < 0.01). Decrease of AVP level was also observed, but did not reach the statistical significance. NT did not change both before and after the treatment. These data suggest that beta-EP and LEK may be involved in pathogenesis of hypertension and in hypotensive action of clonidine.
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PMID:[Changes in plasma neuropeptides before and after clonidine in patients with essential hypertension]. 824 25

Blood pressure stability is better during cold hemodialysis (HD). This has mainly been attributed to a more pronounced sympathetic activation during cold than during warm HD. The authors studied the effect of dialysate temperature on vasoactive peptides, noradrenaline (NA), and renin (PRA). Ten hemodynamically stable patients were dialyzed for 240 min with each of two dialysate temperatures: 38.5 degrees C (warm HD = WHD) and 34.5 degrees C (cold HD = CHD). A decrease (P < 0.05) in blood pressure occurred during WHD; however, during CHD, blood pressure was stable. There were no differences in vasoconstrictors between the two regimens. There was a decrease in NA (P < 0.05), a tendency of PRA to increase (NS owing to a large statistical spread), while arginine vasopressin was unchanged. During CHD, there was a small increase in neuropeptide Y (NPY); however, during WHD, NPY only tended to increase. However, the relative NPY levels (percent of baseline levels) after WHD and CHD did not differ. The vasodilator response was similar during both treatments. Calcitonin gene related peptide was unaltered. Motilin tended to decrease initially, but then increased (P < 0.05) to baseline levels. An increase occurred in beta-endorphin (P < 0.05) and substance P(P < 0.01). There was an initial rise (P < 0.05) in vasoactive intestinal peptide (VIP), followed by a tendency to decrease during the remainder of treatment. The authors concluded that blood pressure stability was better during CHD. However, this was not reflected by differences in plasma levels of the vasoactive peptides, nor did they find any difference in the sympathetic drive between the two regimens.
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PMID:Dialysis fluid temperature and vasoactive substances during routine hemodialysis. 855


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