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)

Plasma ACTH (normal value: 0.16 plus or minus mU/100 ml) was measured in 116 patients with Cushing's syndrome, using a bioassay including dynamic tests and sequential determinations. In 10 patients with adrenal tumors ACTH levels were nondetectable (ND) or low, and usually nonstimulatable. In 10 patients with ectopic ACTH secretion high levels (0.42 plus or minus 0.07 mU/100 ml) were measured. The extracts of 6 tumors yielded an ACTH-like substance. Forty-three patients with Cushing's disease (without pituitary tumor) had, before treatment, a mean ACTH level of 0.18 plus or minus 0.01 mU/100 ml, accompanied by high levels of plasma cortisol (32.1 plus or minus 1.9 mug/100 ml). Irregular nycthemeral variations occurred. ACTH rose to 0.30 mU/100 ml after incomplete adrenalectomy (20 patients) and to 1.14 mU/100 ml after total adrenalectomy (21 patients). Dexamethasone (8 mg per day) suppressed ACTH levels. Metyrapone induced a normal ACTH rise, but at abnormal times. Lysine-vasopressin (LVP) induced an ACTH mean relative increase of 120% before, and of 140% after adrenalectomy (i.e., within the normal range). Six nonadrenalectomized patients with pituitary tumors showed similar abnormalities of ACTH regulation. However, the ACTH rise after LVP was above 500%. When pituitary tumors occurred after adrenalectomy (12 patients) the mean basal ACTH level was 18 mU/100 ml. Dexamethasone induced a 90% decrease, and LVP a 416% increase in ACTH levels. In 6 patients with nodular adrenal hyperplasia, ACTH was undetectable before treatment. After adrenalectomy, ACTH rose to 0.4 mU/100 ml (11 patients) and the increase after LVP was 90%. Five additional patients developed pituitary tumors. These data confirm the abnormalities of ACTH feedback regulation in Cushing's disease. However, even when pituitary tumors occur, ACTH levels can be altered by metyrapone, dexamethasone and LVP. This last test is of particular interest for the detection of pituitary tumors. The follow-up pattern of treated nodular adrenal hyperplasia appears to be very similar to that of Cushing's disease.
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PMID:Studies of ACTH secretion control in 116 cases of Cushing's syndrome. 16 70

The physiological regulation of the plasma corticosteroid concentration, measured by competitive protein-binding, was studied in female rhesus monkeys (M. mulatta) sedated with phencyclidine hydrochloride. Morning basal levels of plasma corticosteroids were found to be in the range 8-0-25-2 mug/100 ml, which is lower than that previously reported in this species. A circadian rhythm in plasma cortisol concentration was demonstrated. Prolonged sedation with phencyclidine was associated with a gradual increase in the plasma cortisol concentration. Synthetic alpha1-24 adrenocorticotrophic hormone given intravenously caused a rapid rise in plasma cortisol, the minimum effective dose was between 1 and 10 ng/kg body weight and the response was maximal after 1000 ng/kg. The administration of lysine-vasopressin and the induction of hypoglycaemia by insulin were both followed by an increase in the plasma corticosteroid concentration. Metyrapone caused a decline in plasma 11-hydroxycorticosteroids and a concomitant increase in total corticosteroids measured by competitive protein-binding. It is concluded that the hypothalamic-pituitary-adrenal system in the rhesus monkey functions in a manner which is qualitatively and quantitatively similar to that of man.
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PMID:Studies on plasma corticosteroids in the rhesus monkey (Macaca mulatta). 81 35

Renal clearances and plasma antidiuretic hormone (ADH), 17-hydroxycorticoids, and norepinephrine were measured in unrestrained dogs before and during exposure to ambient cold (minus 4 to + 4 degrees C). Some dogs were treated with an inhibitor of cortisol biosynthesis, Metopirone, either alone or combined with dexamethasone, a potent glucocorticoid suppressing ACTH release. Plasma ADH increased in the Metopirone-treated group (P smaller than 0.02) but changed little in other dogs. Plasma 17-hydroxycorticoids in untreated dogs rose from a control value of 14.4 plus or minus 1.9 (SE) to 1.82 plus or minus 1.2 mug/100 ml after 20 min of exposure (P smaller than 0.01), an increase comparable with that previously observed in restrained dogs. Plasma norepinephrine increased from 0.98 plus or minus 0.07 to 1.15 plus or minus 0.08 mug/liter (P smaller than 0.01) after 20 min of exposure. Urine flow, C-Cr, and C-PAH tended to increase spontaneously in nonexposed control dogs. Exposure to cold abolished or reversed this tendency, most distinctly in the Metopirone-dexamethasone group. The urine concentration, measured as T-c-H2O/C-Cr, did not change in cold, in contrast to a decrease previously observed in restrained dogs. The data do not support the key role of plasma cortisol elevation in the mechanism of urine-concentration defect in cold and demonstrate important differences between responses of restrained and unrestrained animals.
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PMID:Plasma hormone and renal function changes in unrestrained dogs exposed to cold. 111 60

This paper reviews chemical models of epilepsy and their relevance in the identification and characterization of anticonvulsants. For each convulsant we discuss possible modes of administration, clinical type(s) of seizures induced, proposed mechanism(s) of epileptogenesis and, where available, responsiveness of the induced seizures to anticonvulsants. The following compounds are reviewed: pentylenetetrazol, bicuculline, penicillin, picrotoxin, beta-carbolines, 3-mercaptopropionic acid, hydrazides, allylglycine; the glycine antagonist strychnine; gamma-hydroxybutyrate; excitatory amino acids (glutamate, aspartate, N-methyl-D-aspartate, quisqualate, kainate, quinolinic acid); monosubstituted guanidino compounds, metals (alumina, cobalt, zinc, iron); neuropeptides (opioid peptides, corticotropin releasing factor, somatostatin, vasopressin); cholinergic agents (acetylcholine, acetylcholinesterase inhibitors, pilocarpine); tetanus toxin; flurothyl; folates; homocysteine and colchicine. Although there are a multitude of chemical models of epilepsy, only a limited number are applied in the routine screening of potential anticonvulsants. Some chemical models have a predictive value with regard to the clinical profile of efficacy of the tested anticonvulsants. Some chemical models may contribute to a better understanding of possible mechanisms of epileptogenesis.
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PMID:Chemical models of epilepsy with some reference to their applicability in the development of anticonvulsants. 139 44

A synthetic oligodeoxynucleotide encoding the vasopressin peptide was ligated to the 3' terminal codon of sacB, the structural gene of levansucrase. This gene fusion was integrated into the chromosome of a Bacillus subtilis strain able to overproduce levansucrase. The extracellular production of the hybrid protein, consisting of the whole levansucrase primary sequence plus the nine amino acids of the vasopressin peptide added at the C-terminal end, represented 50-55% of that found for the wild-type levansucrase (20 mg l-1). The purified hybrid protein displayed the same conformational stability, protease insensitivity and enzymic properties as the wild-type levansucrase. However, the rate and the yield of the unfolding-folding transition at the pH and temperature used for bacterial growth were lower in the case of the hybrid protein; the latter also required a higher iron concentration to be completely folded.
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PMID:Peptide carrier potentiality of Bacillus subtilis levansucrase. 152 90

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

The kinetics of binding and endocytosis of 125I-human holotransferrin by isolated human brain capillaries was examined using this system as a model of the human blood-brain barrier (BBB). Both binding and endocytosis of the peptide by human brain capillaries was temperature-dependent and the binding was saturated by holotransferrin, but not by insulin, somatostatin, or vasopressin. Scatchard analysis of the binding reaction revealed a dissociation constant of 448 +/- 110 ng/mL (5.6 +/- 1.4 nmol/L) and a maximal binding constant (Ro) of 8.0 +/- 1.5 ng/mg protein. Thus, the affinity and capacity of the BBB transferrin receptor is within the same order of magnitude as the affinity and capacity of the BBB receptors for insulin, insulinlike growth factor-I, or insulinlike growth factor-II. The human brain capillary transferrin receptor was also detected with a mouse monoclonal antibody to the receptor using the avidin/biotin/peroxidase technique. In conclusion, these studies characterize the human BBB transferrin receptor and support the hypothesis that this receptor acts as a transport system which mediates the transcytosis of transferrin-bound iron through the brain capillary endothelial cell in man.
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PMID:Human blood-brain barrier transferrin receptor. 330 81

Techniques are described in detail for a radioimmunoassay of plasma adrenocorticotropin (ACTH) that is capable of detecting hormone in unextracted normal human plasma at 1:5 dilution under the conditions described. The sensitivity of the assay is at the level of 1 mumug/ml (equivalent to 0.014 mU/100 ml). In normal subjects ACTH concentrations averaged 22 mumug/ml (equivalent to 0.308 mU/100 ml) plasma at 8-10 a.m. In a smaller group the concentrations averaged 9.6 mumug/ml (equivalent to 0.134 mU/100 ml) at 10-11 p.m. Although a circadian rhythm in normal subjects was not always well marked throughout the daytime hours, plasma ACTH usually fell to its lowest value in the late evening. In hospital patients who were not acutely ill, concentrations were infrequently above 100 mumug/ml in the morning and usually fell to significantly lower levels in the late evening. Severely ill hospital patients occasionally exhibited a.m. concentrations above 200 mumug/ml. In a group of subjects showing frequent spiking of plasma 17-OHCS concentrations throughout the day parallel spiking of plasma ACTH as well was generally observed.Metyrapone produced marked increases in plasma ACTH within 24 hr in all cases and generally within 3-6 hr except when started late in the day. Dexamethasone brought about a persistent reduction in plasma ACTH in a patient under continued treatment with metyrapone.Hypoglycemia, electroshock, surgery under general anesthesia, histalog and vasopressin administration were usually followed by significant increases in plasma ACTH concentration. Prior administration of dexamethasone blocked the response to hypoglycemia. Marked elevations in plasma ACTH were observed in patients with adrenal insufficiency off steroid therapy, in Cushing's disease after adrenalectomy even in the presence of persistent hypercortisolemia, and in some untreated patients with Cushing's disease. Umbilical cord blood contained higher plasma ACTH concentrations than maternal blood at delivery in seven of eight cases. After suppression of ACTH secretion by dexamethasone or cortisol. ACTH disappeared from plasma with half-times ranging from 22 min to 30 min in three cases studied.
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PMID:Radioimmunoassay of ACTH in plasma. 430 80

The vasopressin test gave pathological results in 12 cases of optic atrophy and normal results in three cases. One of the patients with a pathological response had Leber's disease and three had tobacco-alcholic amblyopia, while in the rest the optic atrophy was of uncertain origin. In the cases with normal results the aetiology was also unclear. The Metopirone test was normal in 13 cases and pathological in only one case of optic atrophy. In three out of five patients with optic neuritis the vasopressin test gave pathological responses. The high frequency of pathological vasopressin tests in patients with optic lesions indicates a simultaneous disturbance of the hypothalamo-hypophyseal function. The background to this might be a disturbed vascular supply. The vasopressin test was of no help in diagnosing tumours as a cause of optic atrophy.
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PMID:Vasopressin test in cases of optic atrophy and optic neuritis. 555 97

The first half of this manuscript is devoted to a review of the methods used and the results obtained in the published measurements of the normal responses to tests of the three main types of hypothalamic-pituitary-adrenocortical (HPA) activity in man. These are, I, basal, unstressed activity leading to appropriate levels of total daily production of cortisol in the characteristic circadian pattern; II, responses to feedback stimulation of HPA activity by metyrapone administration; and III, responses to tests of the effects of stress on the HPA system including the effects of hypoglycemia, induced fever, vasopressin administration, and ACTH injections and infusions. The advantages and shortcomings of each type of procedure are discussed. The second half of this paper describes the authors' attempts to establish the limits of normality of standard and modified methods of evaluating the HPA system. The defined limits of normality have been used to assess the HPA function in 158 patients with known or suspected disorders of the HPA system. In normal controls, halfhourly plasma cortisol determinations established the normality of circadian and postprandial fluctuations and of mean plasma cortisol concentration, 6.2 +/- 0.3 (SEM) micrograms/dl, which were closely approximated by determinations every 6 h. Metyrapone, given in a dose of 500 mg every 2 h for 24 h increased urinary 17-OHCS excretion to 10.5-32.6 mg/day or to 1.7-7.8 times basal excretion rate. Increasing rates of insulin infusion disclosed significant relationships between resulting plasma glucose and cortisol concentrations. The slopes of the delta cortisol/delta glucose responses were similar after insulin infusions (0.46 +/- 0.05) and after insulin injections, 0.15 U/kg (0.43 +/- 0.09), and were always greater than 0.20 micrograms/mg. This index provides a useful objective measure of the normality of responses to hypoglycemic stress, 0.20-0.87 micrograms/mg. Adrenocortical responses to iv infusions of ACTH (cosyntropin 0.25 mg) may be equivocal at 2 h but are clear cut at 4, 6 and 8 h. Of 158 patients in whom hypopituitarism was known or suspected because of the presence of a pituitary tumor, acromegaly, hyperprolactinemia, or clinical features, HPA function was found to be entirely normal in 88 patients and partially or severely abnormal in the remaining 70 patients.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Normal and abnormal function of the hypothalamic-pituitary-adrenocortical system in man. 608 18


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