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 vasopressin was measured in seven insulin-treated diabetics during 24 h of insulin withdrawal to determine: 1) if abnormalities of the neurohypophysial-renal axis contribute to the dehydration of uncontrolled diabetes mellitus; and 2) the factors causing elevated levels of vasopressin in diabetic ketoacidosis. During the 24 h period of insulin withdrawal, blood glucose rose from 6.7 +/- 1.0 to 20.7 +/- 2.4 mmol/l, whereas plasma vasopressin was 3.6 +/- 0.5 pg/ml initially and in four patients showed little change. Markedly elevated levels of plasma vasopressin (17.8, 19.8 and 26.6 pg/ml) were observed in three patients following the onset of hypovolaemia, nausea and/or vomiting which are known to stimulate vasopressin release. Free water clearance was negative throughout the study in all patients. Thirst was not noted despite marked hyperglycaemia (16.9 +/- 2.5 mmol/l) until a significant fall in body weight of 0.9 +/- 0.2 kg had occurred (p less than 0.005). We concluded that marked elevation of vasopressin results from non-osmotic stimulation and that the mechanisms of body water conservation are overridden by the glycosuric diuresis.
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PMID:Plasma vasopressin during insulin withdrawal in insulin-dependent diabetes. 702 Dec 77

Synthetic arginine-vasopressin (AVP), oxytocin (OXY) and arginine-vasotocin (AVT) were labelled with radioiodine at a moderate specific activity. The purity of the labelled octapeptides was checked by descendent paper chromatography in butanol-acetic acid-water (4 : 1 : 5 v/v) after a double filtration on a Sephadex G-25 column of the labelling mixtures. The rabbit anti-AVP serum bound 125I--AVP, the highest binding belling observed on the descendent eluates from the Sephadex column. The antiserum is specific to AVP, no binding being observed will AVT or oxytocin. The sensitivity of a RIA system using 125I--AVP, commercial anti-AVP serum and polyethyleneglycol separation technique, was of 5 pg/ml in terms of AVP with a biological activity of 385 IU/mg. The validity of the assay was tested on five patients (two with diabetes inspidus (DI) and three with other endocrine diseases) submitted to dehydration of hydration tests.
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PMID:Labelling of octapeptide neurohormones for in vitro studies. Radioimmunologic assay for arginine-vasopressin. 729 46

Vasopressin (Pitressin) infusion through peripheral veins is a commonly used modality for control of bleeding esophageal varices. In this report we describe the development of infected gangrene at the site of accidental vasopressin infiltration in a patient with diabetes mellitus, cirrhosis and bleeding esophageal varices. Among the explanations for the development of gangrene are: 1. continuous intravenous administration; 2. diabetic peripheral vascular disease; 3. mechanical compression of extravasated fluid in a closed space. No antagonist has been clinically proven to reverse the vasoconstrictive effects of vasopressin.
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PMID:Infected gangrene. A serious complication of peripheral vasopressin administration. 741 38

The rare association of diabetes mellitus and vasopressin sensitive diabetes insipidus found in 5 patients attending the Institute of Endocrinology and Metabolic Diseases in a ten-year period is reported. Suspicious signs and criteria for diagnosis were discussed and a brief review made on the pathogenesis and treatment of this association.
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PMID:Diabetes mellitus and vasopressin sensitive diabetes insipidus. 744 14

Transcellular shifts of water and changes in the physiology of water excretion are common in diabetes mellitus and its treatment. Recent evidence indicates that hyperglycemia in diabetic patients, but not in normal subjects, is characterized by elevations of circulating levels of arginine vasopressin (AVP; antidiuretic hormone, ADH). The role and importance of these observations remain to be defined since elevations of plasma AVP levels do not decrease water excretion in diabetic patients. Certain oral sulfonylureas, notably chlorpropamide and tolbutamide, are known to decrease renal free water clearance (CH2O), whereas insulin increases CH2O; the insulin and tolbutamide effects may be clinically trivial, whereas that of chlorpropamide is important. The hyponatremic effect of chlorpropamide may be exaggerated in diabetic patients by concomitant diuretic therapy. Euglycemia during chlorpropamide therapy appears to allow full expression of the action of chlorpropamide on CH2O; hyperglycemia with attendant osmotic diuresis protects chlorpropamide-treated patients against hyponatremia. Inhibition of prostaglandin synthesis with nonsteroidal anti-inflammatory agents enhances expression of the ADH effect on the kidney, but it does not appear to potentiate chlorpropamide hyponatremia. Two other oral sulfonylurea agents, tolazamide and glyburide, increase CH2O. Diazoxide is an antihypertensive thiazide which is antidiuretic as well as hyperglycemic. Thus, abnormalities of water metabolism are common in diabetes mellitus. Whether certain of these abnormalities are clinically important depends upon the presence of the osmotic diuresis of hyperglycemia and the pharmacology of diabetic management.
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PMID:Water metabolism in diabetes mellitus. 745 88

A seventy-four-year-old woman with arteriosclerosis obliterans, diabetes mellitus, and hypertension was admitted for the treatment of intermittent claudication and coldness and pain in the right lower extremity. After the administration of a vasopressin V1 antagonist, OPC21268, the symptoms were markedly improved. Furthermore, blood flow in the dorsalis pedis artery and the cutaneous temperature in the right foot increased in response to acute and chronic administration of OPC21268. OPC21268 may be a new useful therapeutic tool for the treatment of arteriosclerosis obliterans.
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PMID:Improved skin blood flow and cutaneous temperature in the foot of a patient with arteriosclerosis obliterans by vasopressin V1 antagonist (OPC21268). A case report. 748 24

There is an increasing interest on one of the smallest human chromosomes as it is shown by the First International Symposium on the Human Chromosome 20 and by the genetic map prepared by EUROGEN. The conserved part of the long arm of human chromosome 20 is synthenic with the distal part of the mouse chromosome 2 allowing for some analogies between them. Human chromosome 20 contains several important genes for the human pathology. Mutations of one of them, the vasopressin-neurophysin II gene, are responsible for hereditary neurohypophyseal diabetes insipidus. Severe combined immunodeficiency due to adenosin deaminase deficiency is the first human disorder successfully treated by somatic gene therapy. Spongiform encephalopathies are related to mutation and/or polymorphisms of the PRNP amyloid gene. One form of benign familiar neonatal convulsions is mapped to a specific locus on chromosome 20. In some families, maturity onset diabetes of the young (MODY) is caused by alterations of a hypothetical gene closely linked to the ADA locus. Allegile syndrome is often associated with deletions and microdeletions of the short arm of the chromosome. Finally, deletions of the long arm of the chromosome is a frequent finding in several hematologic malignities, specifically in myeloproliferative disorders and myelodysplastic syndromes.
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PMID:[The human genome--chromosome 20]. 748 83

Exercise induces profound changes in the renal hemodynamics and protein excretion. Strenuous exercise provokes a major fall of the renal plasma flow and a reduction of the glomerular filtration rate. Despite these changes, the filtration fraction doubles at maximal exercise preserving the transfer of metabolites or substances through the glomerulus. A higher production of vasopressin and aldosterone enhances the tubular processes of water and electrolyte reabsorption, stabilising therefore the homeostasis during exercise. Urea, uric acid and lactate reabsorption are also increased. Postexercise proteinuria is directly related to the intensity of exercise rather than to its duration. This transient state may be explained by an increased glomerular membrane permeability and a partial inhibition of tubular reabsorption of plasma proteins. Postexercise proteinuria appears to be age-dependent. Exercise has an additional effect on protein excretion in patients with nephropathies (diabetes, renal diseases, kidney transplants).
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PMID:[Renal response to exercise in healthy and diseased patients]. 763 Apr 70

1. To investigate the mechanism of hepatic V1a vasopressin receptor down-regulation in streptozotocin-induced diabetes mellitus in the rat, we measured hepatic V1a receptor mRNA by in situ hybridization histochemistry using oligonucleotide probes to the V1a receptor and Northern blotting. 2. Diabetes mellitus caused hyperglycaemia, hyperosmolality and increased plasma vasopressin concentrations (P < 0.01). Hepatocyte V1a receptor mRNA was reduced by 76% in diabetic rats (P < 0.01) and by 53% in insulin-treated diabetic rats (P < 0.01) versus control rats, in parallel with reduced V1a radioligand binding and vasopressin-stimulated inositol phosphates production. There was a similar decrease in hepatic V1a/18S mRNA density ratio in the diabetic and diabetic+insulin groups (both P < 0.05 versus control). 3. These findings suggest that altered V1a mRNA transcription is responsible for the reduced hepatic V1a receptor density in diabetes mellitus.
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PMID:Down-regulation of vasopressin V1a receptor mRNA in diabetes mellitus in the rat. 763 50

Enhanced cholinergic and dopaminergic controls of anterior pituitary function have been described in insulin-dependent diabetes mellitus (IDDM). In order to verify whether similar neurotransmitter alterations also affect the regulation of posterior pituitary hormone secretion, the arginine-vasopressin (AVP) responses to the dopaminergic agonist apomorphine and in a different occasion to physostigmine, an acetylcholinesterase inhibitor, were evaluated in normal (n = 10) and type I diabetics (n = 16). In addition, a control test with normal saline was performed in all subjects. None of the diabetic patients were affected by neuropathy or other diabetic complications. They were divided into two groups according to the duration of their disease (less than 10 years: group 1, n = 8; more than 10 years: group 2, n = 8). Physostigmine (12.5 micrograms kg-1) was infused intravenously over 10 min; apomorphine (60 micrograms kg-1) was injected subcutaneously. Basal AVP concentrations were similar in all groups and remained constant during the control test. In contrast, both drugs induced significant increments in plasma AVP levels in the normal controls and diabetic subjects. However, physostigmine- and apomorphine-induced AVP increments were twofold higher in diabetics than in control subjects. No significant differences were observed between diabetics of groups 1 and 2. No significant correlations between duration of diabetes and peak AVP responses to physostigmine or apomorphine were found within each group or when all diabetic subjects were considered together. These data indicate enhancement of both dopaminergic and cholinergic stimulatory regulations of AVP secretion in patients with uncomplicated IDDM, regardless of the duration of diabetes.
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PMID:Dopaminergic and cholinergic control of arginine-vasopressin secretion in type I diabetic men. 765 19


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