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

To determine the role of reflex neural mechanisms for hormonal, metabolic, heart rate (HR), and blood pressure (MABP) changes during static exercise, seven health young males performed 10-min periods of two-legged static knee extension both during control and during epidural anesthesia. Comparisons were made at identical absolute (29 Nm) and relative [15% maximal voluntary contraction (MVC)] force. Afferent nerve blockade was verified by hypesthesia below T10-T12 and attenuated postexercise ischemic pressor response. Leg strength was reduced to 67 +/- 5% of control. At same relative force, increases in MABP and HR occurred more rapidly without than with epidural anesthesia (P less than 0.05). This difference was diminished during identical absolute force. Changes in plasma concentrations of catecholamines followed the pattern of HR and MABP responses, with differences between epidural and control experiments being most pronounced early in the work period. Plasma beta-endorphin was elevated only after control exercise. No response at 15% MVC was found for growth hormone, adrenocorticotropic hormone, insulin, glucagon, cortisol, glycerol, free fatty acids, or glucose (P greater than 0.05). In conclusion, during static exercise with large muscle groups and moderate relative force, modest changes in plasma hormones and metabolites take place. Furthermore, afferent nervous feedback from contracting muscles is important in regulation of blood pressure, heart rate, and catecholamine responses during static exercise in humans.
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PMID:Hormonal, metabolic, and cardiovascular responses to static exercise in humans: influence of epidural anesthesia. 187 83

The influence of halothane-nitrous oxide anaesthesia and normotensive epidural analgesia (level of sensory block T8-T10), respectively, on the plasma concentrations of adrenocorticotrophic hormone (ACTH), beta-lipotropin (beta-LPH), cortisol, dehydroepiandrosterone (DHA) and aldosterone as well as on the metabolites glucose, lactate and free fatty acids (FFA) was studied in 20 healthy patients who underwent elective orthopaedic procedures on the lower limbs. ACTH and beta-LPH concentrations in plasma rose significantly (P less than 0.001) during halothane-nitrous oxide anaesthesia. DHA secretion closely followed the secretory profile of cortisol. Increased renin levels and increased ACTH release seemed to be responsible for increased aldosterone secretion, intra-operatively. The hormonally induced rise of glycogenolysis and lipolysis did not produce important intra-operative increases in metabolite concentrations in the blood. In normotensive epidural analgesia no significant increase in stress response could be demonstrated, even with low levels of sensory block.
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PMID:A comparison of two types of anaesthesia on the endocrine and metabolic responses to anaesthesia and surgery. 302 43

Our objective was to elicit and characterize somatogastric reflexes in healthy humans. Sustained somatic stimulation by transcutaneous electrical nerve stimulation (TENS) was applied to the skin of human volunteers while simultaneously monitoring their upper gastrointestinal phasic pressure activity, extraintestinal vasomotor indices, and plasma levels of putative humoral mediators of autonomic reflexes. Stimuli were applied either to the hand (C8-T1) or to the upper abdomen (T5-T10) to determine whether impulses at these two dermatomes produce different effects on fed antral phasic pressure activity. TENS resulted in significant reduction (P = 0.007) in antral motility index when applied to the hand and abdomen as compared with sham stimulation. This was associated with an increase in skin conductance and plasma beta-endorphin levels but no change in pulse, blood pressure, or circulating catecholamine levels. No qualitative changes in proximal intestinal pressure activity were detected. Sustained somatic stimuli resulted in reduced postprandial antral phasic pressure activity. The similarity of the responses to TENS applied to the hand and abdominal dermatomes suggests that the induced somatovisceral responses relay predominantly at the cerebral level.
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PMID:Effect of somatovisceral reflexes and selective dermatomal stimulation on postcibal antral pressure activity. 609 77

Reflex mechanisms from contracting skeletal muscle have been shown to be important for cardiovascular, neuroendocrine, and extramuscular fuel-mobilization responses in exercise. Furthermore, because hypoxia results in exaggerated metabolic changes in contracting muscle, the present study evaluated whether enhancement of cardiovascular and neuroendocrine responses by hypoxia during exercise is influenced by neural feedback from contracting muscle. Seven healthy males cycled at 46% maximal O(2) uptake for 20 min both during normoxia and at 11.5% O(2), and both without and with epidural anesthesia (EA; 20 ml 0.25% bupivacain, resulting in cutaneous hypesthesia below T10-T12 and 25% reduction in maximal leg strength). Exercise to exhaustion was also performed at 7.8% O(2). The exercise-induced increases in heart rate; cardiac output; leg blood flow; plasma concentrations of growth hormone, adrenocorticotropin, cortisol, and catecholamines; renin activity; glucose production and disappearance; norepinephrine spillover [2, 190 +/- 341 ng/min (exercise at 11.5% O(2)) vs. 988 +/- 95 ng/min (exercise during normoxia)]; lactate release from and glucose uptake in the leg; and the decreases in plasma insulin and free fatty acids were exaggerated in hypoxia (P < 0.05). In muscle, concentrations of lactate, creatine, and inosine 5'-monophosphate were higher, and those of phosphocreatine were lower after exercise in hypoxia compared with normoxia. The exercise-induced increase in mean arterial blood pressure was not affected by hypoxia, but it was reduced by EA [108 +/- 4 mmHg (control) vs. 97 +/- 4 mmHg (EA); P < 0.05], and the reduction was more pronounced during severe hypoxia compared with normoxia. Apart from this, time to exhaustion at extreme hypoxia, circulatory responses, concentrations of neuroendocrine hormones, and extramuscular substrate mobilization were not diminished by EA. In conclusion, in essence the hypoxia-induced enhancement of systemic adaptation to exercise is not mediated by neural feedback from working muscle in humans.
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PMID:Cardiovascular and neuroendocrine responses to exercise in hypoxia during impaired neural feedback from muscle. 1040 60

Adrenocorticotropic hormone (ACTH)-induced hypertension in the rat is characterized by nitric oxide deficiency. Tetrahydrobiopterin (BH4) is an essential cofactor for the enzyme nitric oxide synthase and glucocorticoids have been reported to reduce cytokine-induced BH4 production. Accordingly we hypothesized that ACTH-induced hypertension would be reversed by BH4 supplementation. Male Sprague-Dawley rats (n = 33) were treated with BH4 in vehicle (10 mg/kg/day i.p.) or vehicle alone (5 mg/kg/day i.p. of ascorbic acid in 4 mM HCl) for 10 days. ACTH (0.2 mg/kg s.c.) or saline daily injection was started 2 days after BH4 or vehicle treatment and continued for 8 days. Systolic blood pressure (SBP) was measured on alternate days using the tail cuff method. Treatment with HCl, ascorbic acid or BH4 alone had no effect on SBP. In saline treated rats, neither BH4 nor its vehicle modified SBP. In ACTH treated rats, SBP was increased in both BH4 (from 128 +/- 6 to 142 +/- 4 mmHg, T0 to T10, P < 0.0005, one way ANOVA) and vehicle groups (from 127 +/- 3 to 158 +/- 7 mmHg, T0 to T10, P < 0.001, one way ANOVA). There was no significant difference in SBP between BH4 + ACTH treated and vehicle + ACTH treated rats. Thus, daily injection of BH4 (10 mg/kg i.p.) failed to prevent the development of ACTH-induced hypertension in rat.
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PMID:Role of tetrahydrobiopterin in adrenocorticotropic hormone-induced hypertension in the rat. 1513 1