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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

Sodium transport per unit tissue is stimulated in dietetically produced cecum hypertrophy of the rat. Presumably this reflects an adaptive process. The possibility was tested whether transport adaptation was mediated by hormones, particularly by the pituitary-adrenal system, Cecum hypertrophy was induced by dissolving polyethylene glycol in the drinking water, and cecal sodium and water net absorption was measured in vivo. In both the adapted and normal mucosa, sodium and water absorption per unit macrosurface or dry weight was increased by aldosterone and decreased by adrenalectomy, hypophysectomy and volume expansion while the decrease following adrenalectomy was reversed by cortisol and the absence of antidiuretic hormone in hereditary diabetes insipidus rats had little effect on absorption. However, none of the test conditions abolished the relatively larger absorption of the adapted compared to the normal mucosa. It is concluded that the hormonal effects were additive but not causally related to transport adaptation.
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PMID:Hormones and the stimulated sodium transport in cecum hypertrophy. 117 May 50

A 20-yr-old male was found to have diabetes insipidus is association with panhypopituitarism but without any focal neurological lesion being identified. He was initially treated with steroid supplements, the features of diabetes insipidus being controlled with a thiazide diuretic. Eighteen months later the patient lost thirst sensation and stopped treatment, subsequently being re-admitted with severe dehydration, oliguria and focal neurological signs. Further investigation, including brain biopsy, confirmed the presence of an atypical pinealoma which was considered inoperable. Measurements of plasma antidiuretic hormone (ADH) and angiotensin II (AII) concentrations during the severe dehydration showed very high levels of AII, but inappropriately low plasma ADH levels for the severity of dehydration. We consider that the evidence obtained from this case supports the view that the oliguria with hypertonic urine present during severe dehydration was due to a direct renal action of the very high AII levels, possibly supplemented by the residual ADH secretion.
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PMID:A case of hypopituitarism with diabetes insipidus and loss of thirst. Role of antidiuretic hormone and angiotensin II in the control of urine flow and osmolality. 117 97

1. Chlorpropamide, carbamazepine and clofibrate have an antidiuretic action in patients with neurohypophyseal diabetes insipidus which is qualitatively similar to that of antidiuretic hormone (ADH). 2. An additive antidiuretic effect is produced by combination of chlorpropamide and carbamazepine with small dosages of ADH. 3. After an immediate and transient antidiuresis, a single intravenous bolus injection of lysine vasopressin given during treatment with chlorpropamide, chlorpropamide with a continuous intravenous infusion of lysine vasopressin, carbamazepine or clofibrate, resulted in increased water diuresis for 12-24 h or longer. 4. This paradoxical diuresis was not observed during treatment with chlorothiazide. 5. It is suggested that the antidiuretic action of chlorpropamide, carbamazepine and clofibrate is localized at the receptor site for ADH in the distal renal tubular cell.
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PMID:Paradoxical diuresis after vasopressin administration to patients with neurohypophyseal diabetes insipidus treated with chlorpropamide, carbamazepine or clofibrate. 119 87

The antidiuretic action of a number of vasopressin analogues has been measured in the rat and man in water diuresis. These analogues had the following categories of structural alteration: a) substitution of -CH2CH2-(dicarba) and -SCH2-(6-monocarba) for the natural -SS- bridge between residues 1 and 6, b) changes in the nature of the C-terminal tripeptide produced by substitution of D-arginine and L-Nalpha-methylarginine for L-arginine in sequence position 8 and L-leucine for proline in position 7, and c) combinations of a and b. In addition, a highly active analogue which results when valine is substituted for glutamine in position 4 was tested. Trained, unanesthetized rats and normal human volunteers were complemented by a volunteer patient with posttraumatic diabetes insipidus (DI) in the total group of experimental subjects. The only change in the C-terminal tripeptide which was associated with a high antidiuretic action was D-Arg substitution. The meArg and Leu analogues showed low to very little activity and no signs of antidiuretic antagonist action. All of the carba analogues showed both high potency and prolongation of antidiuretic action in the following order (for both potency and duration): monocarba + 8-D-Arg greater than 4-Val + 8-D-Arg greater than 8-D-Arg alone, all in deamino form. None of the 8-D-Arg analogues had any side effects on the cardiovascular system, gut, uterus, bladder, etc. The prolongation was such that even with a DI patient refractory to the action of lysine-vasopressin and relatively resistant to deamino-[8-D-Arg]-vasopressin, water turnover could be reduced from untreated levels of 20 to 30 liters/day to less than 2 liters/day with only a single administration of deamino-6-carba-[8-D-Arg]-vasopressin as nose drops. The significance of these structural alterations in the vasopressin molecule for interaction with both antidiuretic and smooth muscle receptors was discussed.
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PMID:Role of the disulfide bridge and the C-terminal tripeptide in the antidiuretic action of vasopressin in man and the rat. 119 61

1. The effects of unilateral nephrectomy on urinary concentration and dilution were studied in Sprague-Dawley rats. To exclude incomplete suppression of antidiuretic hormone, free water formation was also sutdied in rats with congenital diabetes insipidus (Brattleboro strain). 2. Urinary solute-free water formation was similar in Sprague-Dawley and Brattleboro rats. Uninephrectomized animals excreted a water load promptly and diluted their urine to the same degree as control rats. Maximal values for Cwater and TCwater per kidney were higher after nephrectomy, but were similar to those of control rats at comparable rates of fluid delivery to the distal nephron. Renal tissue osmolaity was similar in uninephrectomized and sham-operated animals, indicating that nonantidiuretic hormone-dependent backflux of filtrate was the same in the two groups. The only defect observed in uninephrectomized animals was a small reduction in maximal urine osmolaity. 3. These results demonstrate that free water formation and reabsorption are unaffected by unilateral nephrectomy and suggest that, in the remaining kidney, filtrate reabsorption along the entire nephron increases in proportion to the increment in glomerular filtration.
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PMID:Urinary concentration and dilution after unilateral nephrectomy in the rat. 120 87

The case of a girl with Laurence-Moon-Biedl syndrome without polydactyly is described. Additional features were small stature, diabetes insipidus neurohormonalis and a renal disorder. The diabetes insipidus neurohormonalis was successfully treated with a new vasopressin analogue, DDAVP. The importance of renal studies in patients with Laurence-Moon-Biedl syndrome is emphasized.
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PMID:Laurence-Moon-Biedl syndrome associated with diabetes insipidus neurohormonalis. 121 37

A radioimmunoassay specific for arginine-vasopressin (AVP) developed in recent years has been applied to measurement of urinary AVP during physiological and clinical studies. Daily excretion of AVP was 34 +/- 10 ng (mean +/- SD) in 17 female normals and 69 +/- 45 ng in 17 male normals, this being a significant difference (p less than 0.01). After osmolar load (Carter-Robbins test) hourly excretion of AVP increased significantly in 7 males from 1.3 to 3.1 ng/h and in 6 females from 1.7 to 6.5 ng/h. Again the difference between male and female normals was significant. In both sexes a significant correlation between AVP excretion and either plasma osmolality or free-water clearance was found. When the osmolar load test was performed under constant angiotensin II perfusion in male subjects, their AVP excretion was significantly more elevated; this confirmed in man the hypothesis that angiotensin II is a stimulus to AVP secretion. Preliminary results of AVP excretion and response to osmolar load in diabetes insipidus are reported. Exceedingly high rate of excretion of AVP up to 55 330 ng/24 h have been found in cases of bronchial carcinoma with dilutional hyponatremia.
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PMID:[Clinical application of the radioimmunological measurement of the antidiuretic hormone]. 121 57

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

A radioimmunoassay for [8-arginine]-vasopressin (AVP), previously described (Czernichow et al. 1975) has been used for the determination of antidiuretic hormone in a 4 ml urine sample. AVP is extracted from acidified urine with a cation exchanger (Amberlite CG 50) with an overall recovery of 72%. The blank value measured in extracted samples of urine was 0.29 pg/ml +/- 0.21 (SEM) and calculated by extrapolation of the regression line of the recovery experiment was 0.49 pg/ml. The coefficient of variation within-assay was 13% and between-assay 18%. Addition of the amounts of AVP found in each specimen of urine voided gave results nearly identical to those of the amounts found in 24 h pool of urine, indicating that the assay was not affected by changes in concentration of the other urinary components during the day. The daily urinary excretion of AVP measured in 34 subjects was found to be 34 ng in 17 women and 70 ng in 17 men, a significant difference. Urinary concentration and excretion rate of AVP rose during thirst test and during Carter-Robbins test performed in 13 healthy subjects. In the latter test it was observed that the women displayed a strikingly more pronounced AVP elevation after the osmolar stimulus than the men. In both sexes a significant correlation was found between AVP excretion rate and plasma osmolality as well as free water clearance. Three cases of complete or incomplete diabetes insipidus and potomania could be clearly differentiated according to the total output of AVP during the thirst test. Extremely high values of AVP were found in the urine of 5 subjects with Schwartz-Bartter syndrome associated with bronchogenic tumours.
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PMID:Radioimmunoassay of (8-arginine)-vasopressin. II. Application to determination of antidiuretic hormone in urine. 124 62


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