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)

Three experimental models have been employed to investigate the mechanism of the prolonged bleeding time in patients with von Willebrand's disease (vWd). 1-deamino-8-D-arginine vasopressin (DDAVP), a synthetic analogue of the antidiuretic hormone, was administered to normal volunteers and patients with vWd in order to induce a short-term, endogenous increase of factor VIII procoagulant activity (VIIIAHF), factor VIII-related antigen (VIIIAGN), and Willebrand factor (VIIIVWF); and to investigate the relationship between bleeding time and plasma variations of factor VIII-associated properties. In normal subjects DDAVP administration was followed by a marked increase of VIIIAHF, VIIIAGN, and VIIIVWF; yet the bleeding time remained unchanged. The same parameters were also raised in two groups of patients with vWd. In a third group of patients with severe recessive vWd, factor VIII-associated properties, which were not measurable before the infusion, were unmodified. The bleeding time remained unchanged in all vWd patients. To investigate the effect of the exogenous increase of factor VIII-associated properties, cryoprecipitate was given to ten vWd patients before dental surgery. Despite the marked increase of VIIAHF, VIIAGN, and VIIVWF observed after the infusion, bleeding time was not shortened. Finally, in order to evaluate the hypothesis that factor VIII may exert its effect on primary hemostasis locally in the vessel wall, VIIIAGN and its relationship with the bleeding time were studied by direct immunofluorescence in gum-biopsy specimens obtained in vWd patients before cryoprecipitate infusion. No reaction could be elicited in five patients with severe, recessive vWd, whereas venules and arterioles stained positively in five patients with a moderate form of the disease. Immunofluorescence microscopy was also carried out in specimens obtained after cryoprecipitate at a time when the plasma defects were corrected but the long bleeding time was not modified; no reaction was detectable on the vessel wall of the three patients who were negative before the infusion.
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PMID:Studies on the prolonged bleeding time in von Willebrand's disease. 78 58

The development of a sensitive and specific radioimmunoassay for vasopressin is described. Antibodies were successfully produced following the coupling of synthetic arginine vasopressin with bovine serum albumin carried out with carbodiimide. In order to standardize the assay, the labelled hormone has to be separated twice using a DEAE-Sephadex-A-25 column and thin layer chromatography with cellulose plates. A further condition to obtain a reproducible standard curve is the use of a pure arginine vasopressin checked by cellulose chromatography. Most of the vasopressin batches available do not fulfil this requirement of purity. With the method described, vasopressin can be determined in unextracted human urine. The lower limit of detection is 2 pg/ml. Normal values are in the range of 67.5 +/- 34.3 ng/24 h (kappa +/- SD, n =45). No significant difference of AVP excretion was found between men and women. The usefulness of the assay is demonstrated in patients with hypothalamic or pituitary disorders.
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PMID:The development of a radioimmunoassay for arginine vasopressin. 82 68

The development of a sensitive radioimmunoassay for plasma arginine vasopressin (pAVP) is described. Using this assay, the levels of vasopressin were determined in the plasma of nondehydrated and dehydrated rats after exposure to ether or acceleration stress. Plasma AVP was also determined in rats following nicotine administration. Nondehydrated rats showed no significant changes in pAVP 1, 2, 5, or 15 min after exposure to ether for 1 min. Dehydrated rats, on the other hand, had significantly reduced pAVP after exposure to ether. One group (180-220 g) showed a decline in pAVP of 27% at 2 min (P less than 0.05) and and 47% at 5 min (P less than 0.001) after stress. In a group of larger animals (350-400 g), pAVP levels were reduced by 55% at 1 min (P less than 0.05) and 72% at 2 min (P less than 0.01) after ether stress. A third group (250-300 g) also had significantly reduced pAVP values of 57% (P less than 0.01) 5 min after ether stress but not at 15 min. Nondehydrated rats which were centriguated at -4.1 Gx for 5, 15 or 120 min showed no significant alterations in pAVP. No decrease in pAVP was observed in dehydrated rats centrifugated for 5 min; after 120 min of centrifugation, mean pAVP was reduced by 40% (P less than 0.02) when compared to be noncentrifugated controls. In contrast to either ether or acceleration stress, nicotine provoked a marked rise (P less than 0.005) in pAVP 10 min after injection. From these results it was concluded that ether or acceleration stress does not evoke an increase in the pAVP levels of rats, and furthermore, in dehydrated rats, these stressors will produce a significant decline in pAVP.
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PMID:Reduction in plasma vasopressin levels of dehydrated rats following acute stress. 83 May 44

During the onset of malignant hypertension (MH) in rats treated with deoxycorticosterone trimethylacetate (DOC), plasma arginine vasopressin (AVP) concentrations increase tenfold as a consequence of hypovolemia and hyperosmolality. In benign hypertensive (BH) rats, plasma AVP is increased threefold in comparison with control animals. Plasma renin is markedly suppressed in both BH and MH animals. In MH rats, biologically active AVP antiserum lowers blood pressure (BP) transiently to normal or subnormal levels; in BH rats, a small BP-lowering effect of the AVP antiserum is seen. (Biologically active angiotensin II antiserum does not lower BP in MH rats.) The relationship between the height of BP and plasma AVP concentration in DOC hypertensive rats indicates, when compared with that relationship in diabetes insipidus rats infused with AVP, a marked enhancement of the vasopressor effect of AVP. These findings and the earlier observation of vasopressin-induced vascular damage by Byrom (F. B. Byrom, The Hypertensive Vascular Crisis. London: Heinemann, 1969) strongly suggest that ADH is involved as a vasopressor hormone in the pathogenesis of malignant DOC hypertension.
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PMID:Vasopressor role of ADH in the pathogenesis of malignant DOC hypertension. 84 73

A patient with the syndrome of chronic hypernatremia (serum Na+: mean = 154, range 139-184 mEq/l, n = 30) and hypodipsia due to a hypothalamic injury was studied to evaluate osmolar and baroreceptor control of arginine vasopressin (AVP) secretion. Resting plasma AVP levels measured by radioimmunoassay were inappropriately low for the degree of plasma hyperosmolality: range = less than 0.5-2.1 pg/ml, n = 10, with corresponding levels of plasma osmolality (P osM) greater than 300 m osmol/kg, suggesting either direct damage to the AVP synthesis and storage area or impaired afferent osmoreceptor function. Direct pituitary damage seemed unlikely, since anterior pituitary function was normal by standard testing. The existence of adequate neurohypophyseal stores of AVP was demonstrated by baroreceptor stimulation with the hypotensive agent trimethaphan (Arfonad): plasma AVP rising to 50.0 pg/ml during transient hypotension (BP = 70/0). Osmoreceptor function was evaluated during acute water loading followed by hypertonic saline infusion. During hypertonic saline infusion plasma AVP levels correlated with P osM (R = .87, P less than .01, n = 8), suggesting some residual osmotic regulation of AVP release. The osmotic threshold for AVP release (the x-axis intercept of the plasma AVP-P osM regression line) was not higher than normal. However, the AVP levels throughout this study remained markedly subnormal for the degree of plasma hyperosmolality (maximum plasma AVP = 1.9 PG/ML when P os M = 327 M OSMOL/KG). Since a substantial amount of AVP was released with baroreceptor stimulation, the inadequate rise in plasma AVP level with hyperosmolality indicates that afferent input from the osmoreceptor/thirst area of the hypothalamus is selectively impaired in this patient. These findings directly demonstrate a dissociation of osmoreceptor function from the AVP secretory apparatus in man.
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PMID:Selective osmoreceptor dysfunction in the syndrome of chronic hypernatremia. 84 75

35S-cysteine injected adjacent to the supraoptic nucleus (SON) of the rat is rapidly incorporated into proteins. These 35S-cysteine-labeled proteins in the SON (1-24 h after injection) were separated by polyacrylamide gel electrophoresis, and the distribution of radioactive proteins on the gels was analyzed. 1 h after injection, about 73% of the radioactivity appeared in two peaks (both about 20,000 mol wt). With time, these peaks (putative precursors of neurophysin) decreased, as a 12,000 mol wt peak (containing two distinct neurophysins) increased in radioactivity. Both the 20,000- and 12,000-mol wt proteins are transported into the axonal (median eminence) and nerve terminal (posterior pituitary) regions of the rat hypothalamo-neurohypophysial system. Conversion of the larger precursor protein to the smaller neurophysin appears to occur, in large part, intra-axonally during axonal transport. Six distinct 35S-cysteine-labeled peptides (less than 2500 mol wt), in addition to arginine vasopressin and oxytocin, are also synthesized in the SON and transported to the posterior pituitary where they are released together with labeled neurophysin by potassium depolarization in the presence of extracellular calcium. These data provide support for the hypothesis that the neurohypophysial peptides (vasopressin and oxytocin) and neurophysins are derived from the post-translational clevage of protein precursors synthesized in the SON, and that the conversion process can occur in the neurosecretory granule during axonal transport.
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PMID:Biosynthesis and axonal transport of rat neurohypophysial proteins and peptides. 85 41

The urinary excretion of arginine vasopressin (AVP) was measured by bioassay in normal subjects at rest, on reduced physical activity and on routine everyday activity. The values obtained under rest conditions were all less than 10 mu/24 h with a mean less than 6.6 mu/24 h. Excretion of vasopressin increased with increasing activity, despite free access to water to mean values of 17 mu/24 h and 29 mu/24 h under conditions of reduced and routine every day activity respectively.
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PMID:Normal excretion of vasopressin and the effect of everyday activity. 86 8

Immunoreactive arginine vasopressin (AVP) and arginine vasotocin (AVT) were quantitated in 15 of 17 human fetal pituitary glands early in gestation (11-19 weeks) and in 8 of 9 ovine fetal pituitary glands late in gestation (109-137 days). In 14 of 15 human fetal glands, AVT content exceeded that of AVP. There was a significant rise of AVP (as a percentage of total AVP plus AVT content) with gestational age over the period of 12-19 weeks (P less than 00.01). The ovine fetal glands demonstrated a preponderance of AVP over AVT. The mean AVP and AVT content in the ovine glands was 5.7 +/- 2.9 and 0.8 +/- 0.2 mU/mg gland weight, respectively, compared with the values in the human fetal pitiutaries, 0.8 +/- 0.2 and 1.2 +/- 0.2 mU/mg gland weight, respectively. The relative percentage of AVP and AVT in the ovine fetal pituitaries was 76.0+/- 9.6% and 23.9 +/- 9.6%, respectively, as contrasted to the human fetal glands, 36.7 +/- 2.7% AVP and 63.3 +/- 2.7% AVT. The preponderance of AVT over AVP in the early gestational age mammalian fetus may represent a primative first step in molecular evolution of the neurohypophyseal peptides.
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PMID:Fetal neurohypophyseal arginine vasopressin and arginine vasotocin in man and sheep. 87 Aug 69

The effect of an angiotensin-converting enzyme inhibitor on the circulating levels of angiotensin I, angiotensin II, and arginine vasopressin was studied in dogs subjected to hypotensive hemorrhagic shock. In dogs subjected to hemorrhage but not given the inhibitor, angiotensin II rose 20-fold (from 69 to 1,343 pg/ml of plasma), whereas in dogs subjected to hemorrhage but pretreated with the inhibitor, angiotensin II rose only 2-fold (from 92 to 171 pg/ml of plasma). In the pretreated dogs angiotensin I rose 30-fold (from 108 to 3,232 pg/ml of plasma). There was no statistically significant difference between the vasopressin levels found in the untreated dogs and the levels found in dogs given the inhibitor (1,016 and 1,095 pg/ml of plasma). Of the 15 dogs in the untreated group, five died before retransfusion was completed (four of cardiac failure and one of cardiac arrhythmia); none of the 10 dogs in the inhibitor-treated group died. These observations suggest that the very high levels of angiotensin II observed following severe hemorrhage do not contribute significantly to the increased secretion of vasopressin and that the inhibitor protects against death, possibly by suppressing the very high blood levels of angiotensin II observed following this type of experimental hemorrhagic shock.
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PMID:Effect of angiotensin-converting enzyme inhibitor (SQ 20881) on the plasma concentration of angiotensin I, angiotensin II, and arginine vasopressin in the dog during hemorrhagic shock. 89 Aug 86

In three cases of established cranial diabetes insipidus, the effectiveness of the new vasopressin analogue 1-desamino-8-D-arginine vasopressin (DDAVP) in controlling diabetes insipidus is demonstrated. A single dose of 20 micrograms of DDAVP given intranasally had an antidiuretic action from 16 to 24 hours in the three cases, and 10 micrograms given twice daily intranasally was effective in controlling the diabetes insipidus with no side effects. All the patients preferred this form of therapy to their previous treatment.
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PMID:DDAVP in the treatment of diabetes insipidus: a clinical study. 89 39


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