Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was undertaken to investigate in a prospective randomized way the influence of the benzodiazepine antagonist flumazenil on endocrine stress response and haemodynamic parameters after modified neuroleptanaesthesia. A total of 24 patients (ASA scores I or II) aged between 18 and 60 who were scheduled for major gynaecological surgery, were investigated. For modified neuroleptanaesthesia, midazolam, fentanyl and vecuronium were administered in standardized doses. After extubation, patients of the flumazenil group received initial injections of 0.2 mg flumazenil to antagonize the residual effect of midazolam and additional doses of 0.1 mg per minute until the desired level of vigilance was reached (awareness of person, time and place). In the control group no flumazenil was used. Endocrine stress parameters and haemodynamic parameters were measured at 7 different times, from before induction of anaesthesia up to 60 minutes after the operation. In both groups, a marked increase in endocrine stress response was observed. Adrenaline, noradrenaline, antidiuretic hormone, adrenocorticotropic hormone, cortisol, glucose and lactate, however, were not additionally influenced by the antagonism. No influence of flumazenil on mean arterial pressure, heart rate and arterial oxygen saturation was observed. After modified neuroleptanaesthesia, a careful antagonism of midazolam with small doses of flumazenil is not disadvantageous with respect of endocrine stress response and haemodynamic reactions.
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PMID:[The effect of flumazenil on the endocrine stress reaction following modified neuroleptanesthesia]. 824 Jun 40

Recently, we reported that rats exposed to a single and short session of inescapable footshocks showed alterations in behavioural response to environmental stimuli which developed progressively over a week and remained present for at least 28 days. The aim of the present study was to investigate whether these behavioural changes were accompanied by alterations in the brain-pituitary-adrenal axis. Male Wistar rats were subjected to 10 inescapable footshocks (S) of 6 s duration and 1 mA intensity during a period of 15 min. Control rats (C) were placed in the shock apparatus for 15 min without receiving shocks. The effects of these experimental procedures were studied 14 days later. Exposure to shocks did not affect basal plasma levels of adrenocorticotropic hormone (ACTH) and corticosterone (CORT). However, the novelty-induced ACTH response was increased in S rats as compared to C rats whereas the CORT response did not differ between C and S rats. The ACTH content of the anterior pituitary gland and adrenal weight were not affected by exposure to inescapable footshocks 14 days earlier. Quantitative immunocytochemistry of vasopressin (AVP) and corticotropin-releasing factor (CRF) in the external zone of the median eminence showed that prior footshock exposure increased the AVPi stores to 167% as compared to C rats, whereas CRFi content was not changed. In addition, S rats showed increased mineralocorticoid (MR) and glucocorticoid (GR) receptor binding capacity in the hippocampus as compared to C rats, whereas affinities were not affected. We conclude that a single and short session of inescapable footshocks has long-lasting effects on brain-pituitary-adrenal functioning concomitant with behavioural alterations.
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PMID:Short inescapable stress produces long-lasting changes in the brain-pituitary-adrenal axis of adult male rats. 826 56

This study was undertaken to investigate the influence of the opiate-antagonist naloxone on the endocrine stress response and haemodynamic parameters after modified neuroleptanaesthesia in a randomized, prospective design. A total number of 22 patients (ASA-scores I or II) between 18 and 60 years scheduled for major gynaecologic surgery were included. For modified neuroleptanaesthesia, midazolam, fentanyl and vecuronium were administered in standardized doses. After extubation, patients of the naloxone-group received injections of 2 x 0.1 mg naloxone; in controls, no naloxone was used. Endocrine stress parameters and haemodynamic parameters were measured 7 times before induction of anaesthesia and up to 60 minutes after the operation. In both groups, remarkable increases in adrenaline, noradrenaline, antidiuretic hormone, adrenocorticotropic hormone, cortisol, glucose and lactate took place in the postoperative period. This stress response was comparable in both groups and not increased by naloxone. No significant influence of naloxone on mean arterial pressure, heart rate and arterial oxygen saturation was observed. After neuroleptanaesthesia, a careful opiate antagonism with small doses of naloxone is not disadvantageous with respect to endocrine stress response and haemodynamic reactions.
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PMID:[Endocrine and hemodynamic effects of naloxone following modified neuroleptanesthesia]. 829 47

The diurnal rhythm of corticosteroid secretion is controlled by the suprachiasmatic nucleus (SCN). In rats, plasma corticosteroid levels rise just before the onset of the activity period during the dark phase. Our previous results indicated that vasopressin as a neurotransmitter from the SCN inhibited corticosteroid secretion in the area of the paraventricular/dorsomedial nucleus of the hypothalamus. We hypothesized that during the day the SCN may serve as an inhibitory system for corticosteroid secretion. To investigate this possibility, intact and SCN-lesioned animals were exposed to mild stress in the morning and evening and their plasma corticosteroid levels were monitored. The results indicate that SCN-lesioned animals have higher morning corticosteroid levels and respond both in the morning and evening with higher corticosteroid levels after stress than do intact control animals. We conclude, therefore, that these results indicate an inhibitory role of the SCN on corticosteroid secretion. The apparent discrepancy with the reported stimulatory role of the SCN on adrenocorticotropic hormone secretion is discussed.
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PMID:Suprachiasmatic nucleus lesion increases corticosterone secretion. 832 72

In addition to increasing blood pressure, stimulating aldosterone and vasopressin secretion, and increasing water intake, angiotensin II affects the secretion of anterior pituitary hormones. Some of these effects are direct. There are angiotensin II receptors on lactotropes and corticotropes in rats, and there may be receptors on thyrotropes and other secretory cells. Circulating angiotensin II reaches these receptors, but angiotensin II is almost certainly generated locally by the pituitary renin-angiotensin system as well. There are also indirect effects produced by the effects of brain angiotensin II on the secretion of hypophyseotropic hormones. In the anterior pituitary of the rat, the gonadotropes contain renin, angiotensin II, and some angiotensin-converting enzyme. There is debate about whether these cells also contain small amounts of angiotensinogen, but most of the angiotensinogen is produced by a separate population of cells and appears to pass in a paracrine fashion to the gonadotropes. An analogous situation exists in the brain. Neurons contain angiotensin II and probably renin, but most angiotensin-converting enzyme is located elsewhere and angiotensinogen is primarily if not solely produced by astrocytes. Angiotensin II causes secretion of prolactin and adrenocorticotropic hormone (ACTH) when added to pituitary cells in vitro. Paracrine regulation of prolactin secretion by angiotensin II from the gonadotropes may occur in vitro under certain circumstances, but the effects of peripheral angiotensin II on ACTH secretion appear to be mediated via the brain and corticotropin-releasing hormone (CRH). In the brain, there is good evidence that locally generated angiotensin II causes release of norepinephrine that in turn stimulates gonadotropin-releasing hormone-secreting neurons, increasing circulating luteinizing hormone. In addition, there is evidence that angiotensin II acts in the arcuate nuclei to increase the secretion of dopamine into the portal-hypophyseal vessels, inhibiting prolactin secretion. Central as well as peripheral angiotensin II increases CRH secretion, but there is little if any evidence that angiotensin II mediates the ACTH responses to other stressful stimuli.
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PMID:Blood, pituitary, and brain renin-angiotensin systems and regulation of secretion of anterior pituitary gland. 834 4

We studied the responses of plasma epinephrine, norepinephrine, adrenocorticotropic hormone (ACTH), cortisol, and antidiuretic hormone (ADH) during and immediately after sevoflurane-nitrous oxide anaesthesia supplemented with vecuronium in seven elderly patients (mean 76.6 +/- 1.7 SEM) who underwent major intra-abdominal surgery. The plasma concentrations of norepinephrine, ACTH, cortisol, and ADH increased in response to surgical procedures (P < 0.05). The plasma concentration of ADH increased to a peak concentration of 189.1 +/- 20.7 pg.ml-1 30 min after skin incision (P < 0.05). The plasma concentrations of epinephrine, norepinephrine, ACTH, and cortisol increased to peak concentrations of 408.6 +/- 135.5 pg.ml-1, 635.7 +/- 167.8 pg.ml-1, 222.6 +/- 48.0 pg.ml-1, and 113.6 +/- 67.5 micrograms.dl-1, respectively immediately after tracheal extubation (P < 0.05). We conclude that, in the elderly patients, the responses of stress hormones to major intra-abdominal surgery were preserved during sevoflurane-nitrous oxide anaesthesia sufficient to prevent increases in arterial pressure and heart rate. The strongest responses of epinephrine, norepinephrine, ACTH, and cortisol were elicited immediately after tracheal extubation.
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PMID:Stress hormone responses to major intra-abdominal surgery during and immediately after sevoflurane-nitrous oxide anaesthesia in elderly patients. 839 Mar 30

After acute administration of amphetamine (AMPH), a characteristic behavioral response occurs in the rat, involving increased locomotion and stereotyped licking, grooming, and biting. AMPH administration also activates several neuroendocrine systems, including the pituitary-adrenal axis. Because recent evidence has supported a role for glucocorticoids in modulating the behavioral response to AMPH, the purpose of the present study was to examine the relationship between behavioral and hypothalamic-pituitary-adrenal (HPA) responses to AMPH and determine the physiological substrates responsible for the AMPH-induced release of adrenal steroids. AMPH administration produced the often-reported "inverted-U" shaped behavioral response. Specifically, locomotion was increased by low doses (0.5-1.0 mg/kg, SC) significantly more so than by the highest dose (5.0 mg/kg, SC), which instead elicited intense focused stereotyped movements. Plasma levels of adrenocorticotropic hormone (ACTH) and corticosterone were increased by AMPH in a monotonic dose-response function, with highest levels measured in rats exhibiting the most intense stereotyped behaviors. Plasma ACTH levels then declined 10-30 min after AMPH administration, while AMPH-induced locomotion and stereotyped behavior persisted well beyond this period. In a parallel study, AMPH failed to elevate plasma levels of vasopressin, an important ACTH secretagogue, and AMPH reduced levels of corticotropin-releasing factor (CRF) immunoreactivity in the median eminence, providing indirect evidence of CRF release from this region. AMPH-stimulated ACTH and corticosterone release were prevented by immunoneutralization of CRF.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pituitary-adrenal axis responses to acute amphetamine in the rat. 839 32

Various endocrine responses to 5-hydroxytryptamine (serotonin, 5-HT) agonists were used to assess serotonergic receptor function after chronic treatment with the antidepressants fluoxetine (10 mg/kg), a 5-HT uptake blocker and the norepinephrine uptake blocker desipramine (DMI, 5 mg/kg). Both were injected (i.p.) once a day for 21 days. DOI (5-HT1C/2 agonist, 0-5 mg/kg i.p.) and 6-chloro-2-[1-piperazinyl]-pyrazine (MK-212) (less selective, but predominantly a 5-HT1C agonist, 0-20 mg/kg i.p.) were administered 18 hr after the final antidepressant injection and 30 min before decapitation. Chronic treatment with both fluoxetine and DMI produced a potentiation in most hormone responses to the 5-HT agonists (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-amino-propane HCl (DOI) and MK-212, although there were several differences in individual hormone responses to the two 5-HT agonists. Fluoxetine and DMI potentiated the MK-212- and DOI-induced increase of plasma oxytocin levels and potentiated the effect of DOI on plasma adrenocorticotropic hormone (corticotropin) and prolactin levels. In contrast, the effect of the high dose of MK-212 on plasma prolactin concentration was reduced by both antidepressants. Only MK-212 increased vasopressin levels and this effect was potentiated by fluoxetine, but not by DMI. Fluoxetine also significantly increased the resting level of plasma vasopressin. DMI potentiated the effect of MK-212 on plasma renin concentration. Pretreatment with fluoxetine significantly increased (38%) the Bmax for the 5-HT1C/2 agonist sites ([125I]DOI) in the hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term treatment with the antidepressants fluoxetine and desipramine potentiates endocrine responses to the serotonin agonists 6-chloro-2-[1-piperazinyl]-pyrazine (MK-212) and (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane HCl (DOI). 839 20

We have characterized a specific binding site for angiotensin IV on bovine aortic endothelial cell membranes. Pseudo-equilibrium studies at 37 degrees C for 2 h have shown that this binding site recognizes angiotensin IV with a high affinity (Kd = 0.71; average of two experiments that yielded values of 0.71 and 0.72 nM). The binding site is saturable and relatively abundant with a maximal binding capacity of 0.59 pmol/mg protein (average of two experiments that yielded values of 0.39 and 0.78 pmol/mg of protein). Non-equilibrium kinetic analyses at 37 degree C revealed a calculated Kd of 59 pM (average of two experiments that yielded values of 67 and 50 pM). The binding site displays a high affinity for angiotensin receptors AT1 or AT2. An analysis of specificity showed that the binding site displays a high affinity for angiotensin IV, low affinities for angiotensin II, [Sar1, Val5, Ala8]angiotensin II and does not recognize L-158,809 (5,7-dimethyl-2-ethyl-3-[(2'-(1 H-tetrazole-5-yl)[1,1'-biphenyl]-4-yl)methyl]-3H-imidazo[4, 5-beta]pyridine H2O) and PD 123319 (1-[4-dimethylamino)3-methylphenyl]methyl-5-(diphenylacetyl) 4,5,6,7-tetrahydro-1 H-imidazo[4,5-c]pyridine-6-carboxylic acid). A few unrelated hormones (bradykinin, [Arg8] vasopressin, endothelin-1, atrial natriuretic factor, isoproterenol and adrenocorticotropic hormone) were unable to inhibit any 125I-angiotensin IV binding. The affinities of different structural analogues of angiotensin IV revealed that the N-terminal position is critical for receptor recognition and the C-terminal proline is also important. GTP gamma S and polyvinyl sulfate did not affect the binding, suggesting that the receptor is not coupled to a G-protein. The divalent cations Mg2+ and Ca2+ were shown to diminish the binding of 125I-angiotensin IV. Cross-linking of 125I-angiotensin IV to bovine aortic endothelial cell membranes in the presence of disuccinimidyl suberate, followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) revealed a major band of 186 +/- 12 kDa. The presence in high concentration of this angiotensin binding site on aortic endothelial cells suggest the existence of a novel mechanism involved in the control of vascular tone or vascular permeability.
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PMID:Characterization of a binding site for angiotensin IV on bovine aortic endothelial cells. 856 70

The effect of month-long naltrexone (NTX) treatment at a daily oral dose of 0.5 mg/kg/day was contrasted with placebo (PLC) in a double-blind study with conjoint clinical and biochemical evaluations of therapeutic effects. Modest clinical benefits were achieved with both PLC and NTX, with marginally better overall results following NTX, and degree of improvement appeared to be related to plasma chemical profiles. Massively elevated levels of beta-endorphin were observed in all children with assays using C-terminal antibody but not with an N-terminal antibody assay. In addition, 70% of the children exhibited abnormally low levels of adrenocorticotropic hormone, and smaller subsets exhibited elevated norepinephrine (60%), arginine-vasopressin (50%), and serotonin (20%). The best clinical responders exhibited the clearest normalization of the elevated plasma chemistries, especially in C-terminal-beta-endorphin and serotonin. There was some evidence of therapeutic carry-over effects in both clinical and biochemical measures in those children who received NTX before PLC. The results suggest that NTX only benefits a subgroup of autistic children, who may be identified by the presence of certain plasma abnormalities. These results suggest a possible linkage between abnormal plasma chemistries, especially those related to the pro-opiomelanocortin system, and autistic symptoms.
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PMID:Low-dose naltrexone effects on plasma chemistries and clinical symptoms in autism: a double-blind, placebo-controlled study. 857 Jul 75


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