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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The response has been studied in nine dogs with hyperadrenocorticism due to adrenocortical tumours to the administration of dexamethasone, insulin, lysine-vasopressin and tetracosactide by measuring the changes in plasma cortisol concentration. Administration of dexamethasone did not produce a decrease in the plasma concentration of cortisol in any of these dogs. Administration of insulin caused slight increases in the plasma concentration of cortisol in four out of eight dogs. Lysine-vasopressin increased the plasma concentration of cortisol in eight out of nine dogs, three responded supranomally. Eight out of the nine dogs responded to tetracosactide administration, three responded supranormally, It is concluded that in the dog, in contrast to man, the lysine-vasopressin test cannot be used to differentiate between pituitary-dependent hyperadrenocorticism and hyperadrenocorticism due to an adenocortical tumour. Apparently pituitary ACTH is not completely depleted in dogs with hyperfunctioning adrenocortical tumours.
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PMID:Adrenocortical function tests in dogs with hyperfunctioning adrenocortical tumours. 43 7

Fifteen seconds after intracarotid injection of [125J]-lysine vasopressin, [3H]-ocytocin, tritiated water or [3H]-inulin, the distribution of radioactivity in 18 regions of the rat brain and in the anterior pituitary was determined. Comparing the concentration of the different tracers (in % of injected radioactivity per g brain tissue), it is assumed that a small amount of the labelled neurohormones is taken up by the brain, indicating a penetration of the blood-brain barrier and/or an accumulation within the structures of the barrier system.
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PMID:Indications for a brain uptake of labelled vasopressin and ocytocin and the problem of the blood-brain barrier. 46 64

A simple efficient procedure for extracting and concentrating arginine-8-vasopressin (AVP) from urine has been coupled with a specific and sensitive radioimmunoassay in order to measure antidiuretic hormone (ADH) excretion in normal humans under various physiological stimuli. Antisera have been raised in rabbits injected with lysine-vasopressin (LVP) or AVP coupled with bovine serum albumin. The antiserum selected for the assay which inhibits the antidiuresis induced in the rat by AVP is used at a final dilution of 1 : 50,000 and possesses a high association constant of 1 x 10(11) 1.mol-1. The limit of detection of the RIA system is 0.5 micronUI/ml of urine (1.25 pg). Urinary ADH has been extracted from urine by Miller and Moses method. Mean recovery of added vasopressin averaged 90.2% +/- 11 (SD) and assay of serial dilutions of such extracts showed that they behave in the assay system in the same way as synthetic AVP standards. Moreover comparison of the results obtained by the RIA to those given by the biological method using the ethanol anesthetized rat showed excellent correlation (r = 0.9 p less than 0.001). Under ad libitum fluid and food intake, mean daily urinary excretion of AVP (uncorrected for recovery) determined in 22 subjects was found to be 30.58 +/- 11.64 mU/h with no significant difference between men and women. In response to an oral waterload ADH became undetectable at the peak of diuresis. Following a 16 hr fluid deprivation, ADH rose moderately. A significant correlation has been found between urine osmolality and AVP excretion rate.
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PMID:[Radioimmunoassay of ADH in human urine (author's transl)]. 47 16

The effects of several types of vasopressin analogs that are considered to be resistant to some of the physiologically significant enzymatic systems were investigated utilizing rats trained in a passive avoidance task. Enhancement of avoidance latencies was observed 2, 7 and 13 days after the single learning trial when deamino-carbavasopressins, triglycyl-8-lysine-vasopressin or its des-glycinamide derivative, and deamino-D-arginine-vasopressin were given shortly after the learning trial in the dose of 1 microgram s.c. (8-L-Arginine)deamino-6-carba-vasopressin and (8-L-ornithine)deamino-6-carba-vasopressin were also active in the dose of 0.1 microgram. Lysine vasopressin and its des-glycinamide derivative failed to enhance avoidance latencies in part of the experiments if doses of 0.3--3 micrograms were administered and 7 or 13 day intervals were used between the learning and the test trials. Enhancement of avoidance latencies was also observed, if some of the peptides were injected 20 min but not 120 or 180 min before the test trial. Marked depression of exploratory behavior of rats in an open field was found after s.c. injections of low doses (1--3 micrograms kg-1) of deamino-carba-vasopressins. Higher doses (10--30 micrograms kg-1) induced sleep-like immobility not accompanied by ataxia or catalepsy.
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PMID:Vasopressin analogs: sedative properties and passive avoidance behavior in rats. 47 29

In eight patients with cirrhosis of the liver and portal hypertension an intravenous infusion of lysine vasopressin induced a rapid increase in the plasma level of the fibrinolytic proenzyme plasminogen activator. In contrast, triglycyl lysine vasopressin (glypressin; GVP), in a dose known to lower portal venous pressure, produced no fibrinolytic response. This lack of fibrinolytic response represents an advantage of GVP over lysine vasopressin in addition to its longer in vivo half-life and lower cardiotoxicity. Clinical trials of GVP in the treatment of bleeding oesophageal varices are needed.
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PMID:Effects of lysine vasopressin and glypressin on the fibrinolytic system in cirrhosis. 48 51

1 Synthetic analogues of oxytocin and of lysine-vasopressin with an hydroxyl group in either the L ro D configuration replacing the primary amino group have been tested for biological activity.2 [1-(L-2-Hydroxy-3-mercaptopropanoic acid)] oxytocin ([L-Hmp(1)]oxytocin) was 1.5 to 2 times more potent than oxytocin on the rat uterus in situ, the rat mammary strip and the rat mammary gland in situ and 3 times more potent on the rat isolated uterus.3 The pressor activity of [1-(L-2-hydroxy-3-mercaptopropanoic acid)-8-lysine]vasopressin ([L-Hmp(1), Lys(8)] vasopressin) was 2.2 and the antidiuretic activity 2.1 times that of lysine-vasopressin.4 The [D-Hmp(1)] analogues of oxytocin and vasopressin were much less potent than the [L-Hmp(1)] analogues.5 The responses to oxytocin and its hydroxy analogues in vivo were qualitatively indistinguishable but the pressor and antidiuretic responses to the hydroxy analogues of lysine-vasopressin were prolonged compared with those to the parent hormone.6 The hydroxy analogues of oxytocin and lysine-vasopressin were not inactivated by pregnancy plasma oxytocinase.7 The results are discussed in relation to the importance of the primary amino group for the biological activity and metabolism of the neurohypophysial hormones.
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PMID:Hydroxy analogues of oxytocin and of lysine-vasopressin. 51 8

[7-(Azetidine-2-carboxylic acid)]-oxytocin and -lysine-vasopressin have been synthesised by a (6 + 3) strategy using protected hexapeptide acids with preformed disulphide bridges, and their biological activities have been investigated. All activities were reduced but not to the same extent. In assays of pressor and antidiuretic activity it was observed consistently that the responses to the vasopressin analogue were of shorter duration than responses to lysine-vasopressin of the same amplitude.
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PMID:Synthesis and biological activities of [7-(azetidine-2-carboxylic acid)]-oxytocin and -lysine-vasopressin. 52 Dec 9

[3-(1,4-Cyclohexadienyl)-L-alanine,8-lysine]vasopressin, otherwise known as [3-(2,5-dihydrophenylalanine),8-lysine]vasopressin or [DiHPhe3]lysine-vasopressin, has been synthesized in an attempt to utilize 2,5-dihydrophenylalanine (DiHPhe) to evaluate the contribution of aromaticity in position 3 to biological activity. The analogue has the same primary structure as lysine-vasopressin, except that two additional hydrogen atoms are present on the ring moiety of the phenylalanine residue in position 3. The key intermediate was the protected nonapeptide N-carbobenzoxy-S-benzyl-L-cysteinyl-L-tyrosyldihydrophenyl-L-alanyl-L-glutaminyl-L-asparaginyl-S-benzyl-L-cysteinyl-L-prolyl-N epsilon-tosyl-L-lysylglycinamide that was synthesized stepwise by the solid-phase technique. Deprotection with sodium in liquid ammonia was followed by sulfhydryl oxidation with I2 to give the hormone analogue. [DiHPhe3]lysine-vasopressin exhibited 125--130 units/mg of antidiuretic, 129--132 units/mg of rat pressor, and 6 units/mg of rat uterus contracting activity. To confirm the presence of DiHPhe in the analogue, an enzymatic procedure employing Aspergillus oryzae was developed that liberates in high yield the amino acid residue in position 3 of the posterior pituitary hormone structure. This study should be applicable to other biologically active peptides.
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PMID:[3-(1,4-Cyclohexadienyl)-L-alanine,8-lysine]vasopressin: synthesis and some pharmacological properties. 53 93

Application of a foot shock during the acquisition trial of a one-trial passive avoidance task is associated with a rise in the concentration of serotonin in the hippocampus 24 h after conclusion of the acquisition trial. Carbon dioxide (CO2) induces amnesia for the passive avoidance response when administered immediately upon termination of the acquisition trial. In rats subjected to CO2 treatment following foot shock the rise in hippocampal serotonin is not observed 24 h later. The vasopressin analogue desglycinamide lysine vasopressin attenuates CO2-induced amnesia for the passive avoidance response when given prior to either the acquisition or the retrieval test (24 h after acquisition). This attenuation of the passive avoidance response is associated with a rise in the hippocampal serotonin concentration similar to the one observed in non-amnesic animals. It is suggested that a correlation exists between changes in hippocampal serotonin metabolism and the retrievability of the passive avoidance response.
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PMID:Parallel changes in behaviour and hippocampal serotonin metabolism in rats following treatment with desglycinamide lysine vasopressin. 55 78

Lysine vasopressin (1 microgram/rat SC) administered 1 hr prior to either the acquisition trial or 24 hr retention trial facilitated passive avoidance retention. Amnesia was produced when a single 50 mg/kg (IP) injection of pentylenetetrazol was given immediately following the passive avoidance acquisition trial. A single injection of lysine vasopressin (1 microgram/rat SC) administered 1 hr prior to either the acquisition trial or 24 hr retention trial antagonized the amnesia.
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PMID:Effect of lysine vasopressin on pentylenetetrazol-induced retrograde amnesia in rats. 56 64


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