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)

A study was made of the effect of the antiepileptic carbamazepine on the water metabolism in 13 vasopressin-sensitive and 4 ADH-resistant diabetes insipidus patients. It was found that in 12 ADH-sensitive diabetes insipidus cases the drug decreased the urinary output and the free water clearance, and increased the urinary osmolarity. The diuresis did not change in ADH-resistant diabetes insipidus patients. The investigations suggest that carbamazepine exerts an ADH-like effect, and can be applied with good results in the treatment of ADH-sensitive diabetes insipidus.
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PMID:Anitdiuretic effect of carbamazepine in diabetes insipidus. 115 Mar 63

The effect on water metabolism of 1-deamino-8-D-arginine vasopressin and lysine vasopressin have been studied and compared in 20 vasopressin-sensitive and 2 ADH-resistant diabetes insipidus patients. In every case of ADH-sensitive diabetes insipidus, diuresis decreased and the urinary osmolality increased more markedly and for a longer time with the former than with the latter drug. Both drugs were ineffective in patients with ADH-resistant diabetes insipidus. Administration of 1-deamino-8-D-arginine vasopressin did not cause any side effect. It is concluded that 1-deamino-8-D-arginine vasopressin can successfully be employed in the treatment of ADH-sensitive diabetes insipidus.
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PMID:Treatment of diabetes insipidus with 1-deamino-8-d-arginine vasopressin. 123 63

Blood-perfused isolated dog kidneys demonstrate steady increases in blood flow and in water and sodium excretion which could be attributed to the accumulation of renal prostaglandins in the perfusing blood. This hypothesis was tested by adding indomethacin, a potent inhibitor of prostaglandins synthesis, to the perfusing blood. Indomethacin completely prevented the vasodilation observed in control kidneys, without affecting glomerular filtration rate. Urine volume was not modified but sodium excretion was enhanced while the steady free water clearance increment observed in the control kidneys was depressed by indomethacin. The sum of sodium and free water clearances which, in the absence of antidiuretic hormone, constitutes an index of the part of the filtered load of solutes which escapes proximal tubular reabsorption, was not modified by indomethacin. Finally, indomethacin partially maintained the osmotic cortico-papillary gradient which was abolished after 2 hrs perfusion in control kidneys. These data suggest that prostaglandins accumulation in the blood is probably the major cause of the vasodilation taking place in isolated blood-perfused kidneys. This vasodilation does not account for decreased proximal reabsorption but partially explains the ADH-resistant diabetes insipidus developing in the isolated kidney. Moreover, indomethacin inhibits sodium reabsorption in the ascending limb of Henle's loop and increases water transport in the collecting duct.
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PMID:Effects of indomethacin on renal hemodynamics and on water and sodium excretion by the isolated dog kidney. 123 89

Congenital nephrogenic diabetes insipidus (NDI) is an X-linked inherited disorder characterized by renal resistance to the antidiuretic hormonal action of vasopressin. This study describes the molecular basis of nephrogenic diabetes insipidus in a dog family. Kidney membranes prepared from NDI-affected male huskies were examined for vasopressin binding and response. Compared to membranes from unaffected canines, those from the kidney inner medulla of NDI-dogs possessed normal V2-receptor numbers, but with 10-fold lower affinity for [Arg8] vasopressin (AVP). Adenylate cyclase stimulation by AVP in contrast to that by forskolin or GTP-analogues was similarly reduced in a dose responsive manner. The NDI-affected dogs showed antidiuretic responses to very high doses of V2-specific agonists, consistent with their possessing V2-receptors of lower affinity. Prolonged treatment with V2-agonists, 1-deamino [D-Arg8] VP (dDAVP) and 1-deamino [Val4, Sar7] AVP (dVSAVP), rendered the NDI-affected dogs near normal in terms of water intake and urine osmolality.
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PMID:A low affinity vasopressin V2-receptor in inherited nephrogenic diabetes insipidus. 138 65

Arginine-vasopressin (AVP), interacts with at least two types of receptors: V1 receptors which mediate the aggregating effects of AVP on human blood platelets and other AVP actions on vascular smooth muscle and hepatocytes; and V2 receptors which mediate the antidiuretic effects on renal tubules. Congenital nephrogenic diabetes insipidus (CNDI) is a rare X-linked disorder in humans with abnormal renal and extrarenal V2-receptor responses. However, the V1 receptor responses are apparently normal, since in these patients blood pressure increases in response to AVP. To assess V1 receptor responses, binding studies (3H-AVP) were done on intact platelets obtained from 6 male patients with CNDI, 10 normal subjects and 4 patients with autosomal dominant central diabetes insipidus (ADCDI). The affinity constant (0.68 +/- 0.04 vs. 0.59 +/- 0.06 nM) and the number of specific binding sites per platelet (101 +/- 6 vs. 86 +/- 12) were similar in the normal subjects and the patients with CNDI. However, the number of binding sites per platelet was increased in the patients with ADCDI (189 +/- 12). Platelet aggregation induced by AVP was equivalent in the three groups. Platelet-fraction AVP was elevated in patients with CNDI and undetectable in patients with ADCDI. These results suggest that the structure and the function of V1 platelet receptor-effector pathway are normal in patients with CNDI.
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PMID:Platelet vasopressin receptors in patients with congenital nephrogenic diabetes insipidus. 182 44

Vasopressin-resistant diabetes insipidus is a common side effect of the treatment of affective disorders with lithium. We studied the effect of amiloride on lithium-induced polyuria in nine such patients receiving maintenance lithium therapy who had a vasopressin-resistant defect in urinary concentrating ability. After a mean (+/- S.E.) of 24 +/- 6 days of amiloride administration, the urine volume fell (from 4.7 +/- 0.6 to 3.1 +/- 0.3 liters per 24 hours; P less than 0.005), and the urine osmolality increased (from 228 +/- 35 to 331 +/- 34 mOsm per kilogram of H2O; P less than 0.001). The decrease in urine output was sustained during six months of observation in the absence of any significant change in plasma levels of lithium, potassium, or bicarbonate; urinary excretion of sodium or lithium; or creatinine clearance. Amiloride administration was also associated with a significant increase in urine osmolality (from 575 +/- 54 to 699 +/- 48 mOsm per kilogram of H2O; P less than 0.005) measured after fluid deprivation and the injection of exogenous vasopressin. We conclude that amiloride mitigates lithium-induced polyuria, at least partly, by blunting the inhibitory effect of lithium on water transport in the renal collecting tubule. Thus, amiloride may provide a specific therapy for polyuria in lithium-treated patients while obviating the need for potassium supplementation in the treatment of this kind of polyuria.
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PMID:Amelioration of polyuria by amiloride in patients receiving long-term lithium therapy. 396 96

Congenital nephrogenic diabetes insipidus is a recessive hereditary disorder characterized by the inability of the kidney to concentrate urine in response to vasopressin. Recently, we reported mutations in the gene encoding the water channel of the collecting duct, aquaporin-2 (AQP-2) causing an autosomal recessive form of nephrogenic diabetes insipidus (NDI). Expression of these mutant AQP-2 proteins (Gly64Arg, Arg187Cys, Ser216Pro) in Xenopus oocytes revealed nonfunctional water channels. Here we report further studies into the inability of these missense AQP-2 proteins to facilitate water transport in Xenopus oocytes. cRNAs encoding the missense AQPs were translated with equal efficiency as cRNAs encoding wild-type AQP-2 and were equally stable. Arg187Cys AQP2 was more stable and Gly6-4Arg and Ser216Pro AQP2 were less stable when compared to wild-type AQP2 protein. On immunoblots, oocytes expressing missense AQP-2 showed, besides the wild-type 29 kDa band, an endoplasmic reticulum-retarded form of AQP-2 of approximately 32 kD. Immunoblots and immunocytochemistry demonstrated only intense labeling of the plasma membranes of oocytes expressing wild-type AQP-2. Therefore, we conclude that in Xenopus oocytes the inability of Gly64-Arg, Arg187Cys or Ser216Pro substituted AQP-2 proteins to facilitate water transport is caused by an impaired routing to the plasma membrane.
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PMID:Water channels encoded by mutant aquaporin-2 genes in nephrogenic diabetes insipidus are impaired in their cellular routing. 753 61

Congenital nephrogenic diabetes insipidus (NDI) is a rare inherited disorder characterized by the inability of the kidney to concentrate urine in response to vasopressin (AVP). Following the recent characterization of the cDNA and genomics sequences encoding the human V2 receptor to AVP (AVPR2), X-linked NDI has been found to be due to mutations in the AVPR2 gene that maps to the chromosome Xq28 region. To date more than 30 mutations, insertions or deletions have been reported in independent families, without any significant differences in the phenotypic expression of the disease. The AVPR2 is a member of the superfamily of 7 transmembrane domain, G protein-coupled receptor, linked to cyclic AMP second messenger system. Other types of inheritance have been described in NDI, and recently, a mutation of the aquaporin-2 gene, encoding a water channel of the renal collecting duct, has been reported in an autosomal recessive form of NDI.
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PMID:[Hereditary nephrogenic diabetes insipidus]. 764 Jul 59

Congenital nephrogenic diabetes insipidus (NDI) is an X-linked recessive disease characterized by insensitivity of the distal nephron to the antidiuretic effect of arginine vasopressin. The hypothesis that the defect underlying NDI might be a dysfunctional renal vasopressin V2 receptor has recently been proven by the identification of mutations in the V2 receptor gene in NDI patients. We examined thirteen unrelated Dutch NDI families and identified thirteen distinct and unique mutations. These included nine missense mutations, two nonsense mutations and two small deletions and were found in the extracellular domains II, III and IV, the intracellular domains II and IV and in the transmembrane loops I, II, IV and V of the vasopressin type 2 receptor. In the families with multiple NDI patients the mutated gene cosegregated with the disease. Our data suggest a higher mutation frequency in male than in female gametes. No discrepancies between carrier detection by means of DNA analysis with closely linked polymorphic markers and the definite diagnosis based on sequencing data were found.
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PMID:Inheritance of mutations in the V2 receptor gene in thirteen families with nephrogenic diabetes insipidus. 793 35

Congenital nephrogenic diabetes insipidus is a rare hereditary disease characterized by a renal insensitivity to circulating vasopressin. Genetic linkage studies have demonstrated that the gene responsible for congenital nephrogenic diabetes insipidus is located in region 28 of the X chromosome long arm. That the gene coding for the vasopressin V2 receptor is also located in the q28-qter of chromosome X suggests that the signalisation defect in congenital nephrogenic diabetes insipidus is at the level of the receptor itself. Indeed, congenital nephrogenic diabetes insipidus is a genetically heterogeneous disease since several point mutations in the vasopressin V2 receptor gene nucleotide sequence have been observed in different families of afflicted patients. Moreover, the observation that one of these mutations leads to a lack of cyclic AMP production in response to vasopressin confirms that mutations of the vasopressin V2 receptor sequence are the molecular defects responsible for congenital nephrogenic diabetes insipidus.
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PMID:[Congenital nephrogenic diabetes insipidus]. 793 38


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