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)

The effect of somatostatin (SRIH) on the release of growth hormone (GH) induced by lysine-vasopressin (LVP) was studied in six normal subjects. They were injected intravenously with 0.06 I. U./kg of LVP alone or in combination with SRIH (an intravenous bolus of 100 micrograms 10 minutes before LVP injection, followed by the constant infusion of 500 micrograms over 90 minutes). LVP strikingly increased serum concentrations of GH; this response was significantly reduced by the treatment with SRIH. This finding provides evidence that the effect of LVP on serum GH levels is sensitive to the inhibition by SRIH; it is proposed that the stimulating action of LVP on GH secretion might be mediated by the inhibition of endogenous SRIH.
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PMID:Inhibition by somatostatin of the release of growth hormone induced by lysine-vasopressin in normal subjects. 286 93

Parathyroid hormone (PTH) -degrading activity was studied using osteoblast-like UMR-106 cells. PTH-degrading activity was assessed by the amount of PTH fragments produced in the medium after exposure of intact human PTH-(1-84) to UMR-106 cells. PTH immunoreactivity recovered in trichloroacetic acid-soluble products of the medium and in fractions eluted from reverse-phase high-performance liquid chromatography (HPLC) was measured by radioimmunoassay using an antibody specific for the mid-region and C-terminus of PTH. In this study, intact UMR-106 cells but not extracellular enzymes cleaved human PTH(1-84) into fragments which were released into the medium (in a time- and temperature-dependent fashion). HPLC analysis of the PTH fragments depicted three immunoreactive peaks (peaks 1, 2 and 3) besides intact PTH, indicating a limited PTH-hydrolyzing activity of the cells. Furthermore, a 1000-fold molar excess of either hPTH-(3-34) or [Nle8,Nle18,Tyr34]hPTH-(3-34)amide inhibited PTH-degrading activity by 63% and 80% of control, respectively, whereas neither calcitonin, vasopressin nor growth hormone suppressed it. Additionally, HPLC analysis of the samples treated with [Nle8,Nle18,Tyr34]hPTH-(3-34)amide showed a reduction of the three peaks, suggesting an involvement of PTH receptor in the production of PTH fragments. This PTH-degrading activity was strongly inhibited by phenylmethylsulfonyl fluoride and chymostatin, but not by soybean trypsin inhibitor, elastatinal or inhibitors of cysteine, aspartic or metalloproteinases, indicating that it is due to a seryl chymotrypsin-like endopeptidase. Chymotrypsin-like activity seems to be solely responsible for PTH-degrading activity in intact UMR-106 cells, since all three PTH fragments were predominantly suppressed in the presence of chymostatin. Further analysis of chymotrypsin-digested products of hPTH-(1-84) eluted from HPLC exhibited five fragments detected by ultraviolet absorbance at 210 nm, three of which were measurable by PTH radioimmunoassay, each corresponding to the three PTH fragments produced by UMR-106 cells. To explore the cleavage sites of PTH further, amino acid analysis of chymotrypsin-cleaved products was performed. The results strongly support the view that the chymotrypsin-like enzyme in UMR-106 cells cleaved the hormone between residues 23-24 and 34-35, to produce, at least, hPTH-(24-84) and -(35-84). Our present study indicates that a chymotrypsin-like endopeptidase is solely responsible for limited hydrolysis of PTH by intact UMR-106 cells.
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PMID:Parathyroid hormone degradation by chymotrypsin-like endopeptidase in the clonal osteogenic UMR-106 cell. 291 1

To determine the role of arginine vasopressin (AVP) in stress-induced release of anterior pituitary hormones, AVP antiserum or normal rabbit serum (NRS) was micro-injected into the 3rd ventricle of freely-moving, ovariectomized (OVX) female rats. A single 3 microliter injection was given, and 24 hours later, the injection was repeated 30 min prior to application of ether stress for 1 min. Although AVP antiserum had no effect on basal plasma ACTH concentrations, the elevation of plasma ACTH induced by ether stress was lowered significantly. Plasma LH tended to increase following ether stress but not significantly so; however, plasma LH following stress was significantly lower in the AVP antiserum-treated group than in the group pre-treated with NRS. Ether stress lowered plasma growth hormone (GH) levels and this lowering was slightly but significantly antagonized by AVP antiserum. Ether stress also elevated plasma prolactin (Prl) levels but these changes were not significantly modified by the antiserum. To evaluate any direct action of AVP on pituitary hormone secretion, the peptide was incubated with dispersed anterior pituitary cells for 2 hours. A dose-related release of ACTH occurred in doses ranging from 10 ng (10 p mole)-10 micrograms/tube, but there was no effect of AVP on release of LH. The release of other anterior pituitary hormones was also not affected except for a significant stimulation of TSH release at a high dose of AVP. The results indicate that AVP is involved in induction of ACTH and LH release during stress. The inhibitory action of the AVP antiserum on ACTH release may be mediated intrahypothalamically by blocking the stimulatory action of AVP on corticotropin-releasing factor (CRF) neurons and/or also in part by direct blockade of the stimulatory action of vasopressin on the pituitary. The effects of vasopressin on LH release are presumably brought about by blockade of a stimulatory action of AVP on the LHRH neuronal terminals.
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PMID:Role of arginine vasopressin in control of ACTH and LH release during stress. 298 9

The endocrine function of the thyroid and gonads has for long been investigated using the corresponding releasing hormones (TRH- and LHRH-test, respectively). The adrenal cortex has, up to now, been stimulated using insulin-induced hypoglycaemia or lysine-vasopressin and growth hormone stimulated using arginine. New diagnostic possibilities have arisen with the isolation of the corresponding releasing-hormones, CRF and GRF, and with the availability of these too for clinical use. Using the four above mentioned releasing-hormones in a global pituitary-stimulation-test, the secretion of ACTH, cortisol, STH, TSH, LH, FSH and prolactin hormones can now be examined together.
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PMID:[Global pituitary stimulation test with releasing hormones]. 298 36

The French technique of anaesthesia by electrostimulation described in 1972 by Cara and coworkers, consists of transcranial electrostimulation by means of a high frequency current combined with administration of a neuroleptic drug, a benzodiazepine, a curare and nitrous oxide with oxygen. Fentanyl is also given by some authors. In order to assess the benefit of such electrostimulation, this study compared two randomized groups of ten patients, scheduled for abdominal and pelvic surgery. Both groups received the same drugs (i.e. droperidol, flunitrazepam, pancuronium and nitrous oxide with oxygen), whereas patients in group I were also submitted to electrostimulation. This study describes and discusses the clinical behaviour of patients and the hormonal reactions before, during and after surgery. In both groups, operative conditions were satisfactory. Recovery and onset of spontaneous ventilation were rapid and no patient had an unpleasant recall of the operation itself. However, most of them complained of postoperative pain. Electrostimulation did not reduce the quantity of drugs required during and after surgery. In both groups, circulatory activity was significantly increased. In group I, the arterial pressure and the heart rate were significantly higher than in group II during and after surgery. The hormonal reactions showed that in both groups adrenocorticotrophic hormone, growth hormone and antidiuretic hormone increased during surgery. Adrenocorticotrophic hormone concentration was higher in group I during the operation. The serum levels of cortisol decreased before surgery in group I and rose in both groups during and after laparotomy; prolactin increased before surgery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Electro-drug anesthesia. Clinical and hormonal effects of transcranial electrostimulation]. 299 Feb 60

Thirty two male patients undergoing coronary bypass surgery were given low (group A, 0.01 mg/kg bw) and high dose (group B, 0.035 mg/kg bw) fentanyl anaesthesia. Haemodynamic and hormone responses were investigated from the beginning of anaesthesia until extracorporeal circulation (ECC) (group A: n = 16; group B: n = 16). Significant changes in haemodynamics occurred only in group A including an increase in heart rate (36%) and systolic arterial pressure (21%). Plasma vasopressin (ADH) levels rose significantly in both groups after the beginning or surgical procedure which was markedly less pronounced in patients with high fentanyl (group B). In group A (low dose) a second dose of fentanyl was given after sternotomy, which was followed by a significant decrease in ADH (80% from previous value). No significant variations could be demonstrated in plasma levels of cortisol, ACTH, and human growth hormone (HGH). The data stress the importance of plasma-vasopressin-levels in determining the endocrine stress response following trauma and operation. On the other hand there was a lack of correlation between trauma and pain and frequently reported patterns of the endocrine-metabolic stress response.
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PMID:[Significance of endocrine parameters of stress]. 299 19

This consideration of the influence of endogenous opioid peptide systems on GnRH and oxytocin neurones serves to illustrate some of their possible regulatory interactions with other neuroendocrine systems. Opioids are known to influence the secretion of all the anterior pituitary hormones (see Grossman & Rees, 1983) and these effects are likely to be mediated, at least in part, in the hypothalamus. For example, inhibitory effects of opioids have also been described on secretion from the median eminence of somatostatin (Drouva et al. 1981b) and dopamine (Wilkes & Yen, 1980), and this site of action probably accounts for at least some of the stimulatory effects of exogenous opioids on plasma growth hormone and prolactin levels respectively. For the GnRH neurones the influence of endogenous opioid neurones, possibly the arcuate beta-endorphin system, appears to be mediated indirectly by inhibiting release of excitatory or facilitatory monoamines. This opioid-adrenergic interaction itself appears to be central in the regulation of gonadotrophin secretion and mediation of the feedback effects of gonadal steroids in the brain. The steroids may act directly on both adrenergic and opioid neurones, altering monoamine metabolism and release which may, in turn, regulate numbers of adrenergic receptors perhaps located on the GnRH neurones. Opioid peptide levels are also modulated by steroids probably reflecting altered synthesis and/or processing of precursors. Regulation of the opioid-adrenergic input may not only acutely affect the secretory output of the GnRH neurones but also influence synthesis or processing of GnRH itself (see Kalra & Kalra, 1984) and its degradation by hypothalamic peptidases (Advis, Krause & McKelvy, 1983). Oxytocin neurones demonstrate three further levels of interaction with endogenous opioid peptides. First the anatomical organization of the oxytocin neurones has enabled a clear demonstration of the action of opioids close to the secretory terminals to uncouple the generation of electrical activity from release of peptide. Secondly, both the oxytocin and the neighbouring vasopressin neurones themselves synthesize, process and package opioid peptides. These neurones thus provide a clear example of co-existence of several biologically active products in individual neurones. The relative expression of the different gene products may prove to be a further level of control of opioid influences on the oxytocin and vasopressin neurones.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Endogenous opioid peptides and hypothalamic neuroendocrine neurones. 299 85

A number of alcohol research groups have measured anterior and posterior pituitary hormones, the endogenous opiates, CNS peptides, and putative neurotransmitters during alcohol withdrawal. The data are often complex and contradictory, though a number of themes have emerged. Activity of the hypothalamic-pituitary-adrenal axis (HPA) is increased during chronic alcohol exposure and appears to remain altered for at least 2 to 4 weeks after cessation of drinking. There is increased turnover of norepinephrine and enhanced binding of CNS adrenergic receptors. By contrast, there are decreases in CNS activity of select endogenous opiates and GABA. Other CNS compounds that may play a role in alcohol withdrawal are prolactin, thyrotropin-releasing hormone (TRH), vasopressin, cyclic 3'5'-adenosine monophophate (cAMP), Delta-sleep-inducing peptide (DSIP), and iron. Despite many studies in humans and animals, the roles of CNS dopamine and serotonin in withdrawal remain unclear. A number of peptides, including cholecystokinin (CCK), neurotensin, and bombesin, have been shown to interact with the CNS actions of alcohol and may play a role in alcohol withdrawal. Inadequate work has been performed on acetylcholine (ACh), human growth hormone (HGH) and luteinizing hormone (LH). Studies of the recently identified GABA-benzodiazepine-barbituate receptor complex indicate that this system is likely to be involved in the pathophysiology of alcohol withdrawal. Perturbation studies with corticotropin-releasing factor (CRF) and TRH (with measures of ACTH and cortisol and TSH and prolactin, respectively), may identify patients with withdrawal-related autonomic dysfunction.
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PMID:Clinical neuroendocrinology and neuropharmacology of alcohol withdrawal. 301 Mar 91

Extracellular action potentials were recorded from 48 single units located in the hypothalamic arcuate and ventromedial nuclei. Fifteen percent of the cells were identified as projecting to the median eminence and some of these cells may have belonged to the tuberoinfundibular dopaminergic systems. Responses of all cells to stimulation of the ipsilateral supraoptic nucleus were recorded; 17% of ventromedial nucleus neurons were antidromically identified as projecting to the supraoptic nucleus. None of the latter cells was also identified as projecting to the median eminence. Three of six identified tuberoinfundibular and eight unidentified ventromedial nucleus cells were found to be excited by stimulation of the supraoptic nucleus. One arcuate cell identified as projecting to the median eminence was nonresponsive to supraoptic stimulation. Orthodromic inhibitory responses were recorded from 17% of all cells recorded but no inhibitory responses were recorded from cells identified as projecting to the median eminence. We suggest that these results may provide some neurophysiologic explanations for the observed interrelationships between oxytocin and prolactin secretion, and between vasopressin and growth hormone secretion.
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PMID:Electrophysiologic evidence for connections between the supraoptic and the arcuate/ventromedial hypothalamic nuclei in the rat. 301 86

The sauna induces changes in the secretion of hormones, some similar to changes induced in any other stress situation and others characteristic of exposure to the sauna. Noradrenaline is usually the only catecholamine raised by the sauna in people accustomed to it. The secretion of the antidiuretic hormone is increased and the renin-angiotensin-aldosterone system is activated. The concentrations of the growth hormone and prolactin, in particular, secreted from the anterior pituitary are increased in the circulation. The concentration of the immunoreactive beta-endorphin in blood may also increase which may reflect the feeling of pleasure or, on the other hand, discomfort induced by the sauna. The views on the effects of the sauna on the secretion of the ACTH and cortisol are partly contradictory, probably due to differing ways of taking the sauna bath. In Finnish sauna takers the concentration of cortisol in blood is not usually increased. The changes induced by the sauna in various hormone concentrations in the circulation are, however, normalized within a couple of hours after the heat stress.
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PMID:How the sauna affects the endocrine system. 321 98


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