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)

Hypouricemia in coexistence with hyponatremia often differentiates the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) from most other causes of hyponatremia. We report clearance studies in 5 cases of hyponatremia and hypouricemia that were not due to SIADH. One had metastatic pancreatic carcinoma with ascites, edema, hypoalbuminemia and hypophosphatemia. Two had adenocarcinoma of the lung with metastasis to the brain in 1, 1 had disseminated cryptococcus and 1 had Hodgkin's disease. None received radiation or known nephrotoxins at least 4 months prior to study. None had serum creatinine greater than 106.1 mumol/l (1.2 mg/dl). Two had postural hypotension and hyponatremia that responded to saline therapy. Fluid restriction corrected the hyponatremia in all patients, but the hypouricemia, high fractional excretion (FE) of urate, and high urine sodium concentration persisted. In 2 patients studied, ADH was appropriately suppressed after volume repletion but there was a defect in free water clearance due to high renal solute excretion. In contrast to patients with SIADH who correct their defect in renal urate transport with correction of hyponatremia by water restriction, our patients appear to have a persistent renal urate transport defect and abnormality in sodium conservation. Elevated FE urate of greater than 10% after correction of hyponatremia can thus differentiate these patients from SIADH. The diametrically opposing goals of fluid therapy emphasize the importance of differentiating one group from the other.
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PMID:Hyponatremia and hypouricemia: differentiation from SIADH. 235 Sep 4

The effects of chronic phosphate depletion on vasopressin (ADH) secretion and kidney tissue ADH concentration were examined in rats fed on a diet containing 0.26% phosphorus (LP) or 0.99% phosphorus (NP). The concentration of plasma phosphorus (P) fell significantly in the LP rats after a 4-week period on the experimental diet. There was no significant difference between the LP and NP rats as regards their plasma ADH concentrations and kidney tissue ADH concentrations in normal hydration after a 4-week period on the experimental diets. Following hypertonic saline tests, the plasma ADH concentrations increased significantly in the LP and NP rats, but there was no significant difference between the groups. The kidney medulla and papilla ADH concentrations increased significantly with plasma ADH elevations in both groups. Again, no difference could be found in the cortico-medullary ADH concentration gradients between the two groups. These results indicate that chronic hypophosphatemia in phosphate depleted rats may not be related to ADH secretion and the distribution or tissue concentration of ADH in the kidney. Further, our data suggest that a low plasma P does not influence the ability of ADH to bind to kidney receptor in rats.
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PMID:Effect of phosphate depletion on vasopressin secretion and kidney tissue vasopressin concentration in rats. 235 63

Cytochalasin is known to inhibit the antidiuretic hormone-induced hydro-osmotic response (bulk water flow) in the amphibian urinary bladder without altering hormone-stimulated diffusional water permeability or short-circuit current. In addition, histological studies have shown that the mold metabolite induces the formation of large intracellular vacuoles or lakes in the epithelial cells. We report here a transmission electron microscopic time-course study which indicates that during the early phases of the ADH response cytochalasin causes the formation of numerous multivesicular bodies or aggregates derived from individual basolateral pinocytotic vesicles. Because of their apparent hypertonic nature, the vesicles, as well as the vesicular aggregates, accumulate water during hormone-stimulated hydro-osmotic flow. As a result, the multivesicular bodies dilate and fuse to form the large intracellular lakes characteristic of cytochalasin treatment in the presence of both an applied osmotic gradient and vasopressin. In the presence of mucosal ruthenium red, the luminal glycocalyx was heavily stained with this tracer. At no time, however, even in the presence of hormone, was there any evidence for the uptake of this dye at the apical epithelial border. In the presence of serosal ruthenium red, the lateral intercellular spaces, basolateral pinocytotic vesicles, basal lamina, and collagen, as well as other subepithelial structures, were ruthenium positive. With cytochalasin D, vasopressin, and serosal ruthenium red, both the pinocytotic vesicles and the multivesicular bodies demonstrated an apparent membrane associated ruthenium positive coat. The tracer data indicates that the basolateral pinocytotic vesicles, increased by the presence of hormone, are indeed endocytotic in nature. The mucopolysaccharide coat associated with these structures may be involved in ionic and/or fluid transport.
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PMID:Antidiuretic hormone response in the amphibian urinary bladder: time course of cytochalasin-induced vacuole formation, an ultrastructural study employing ruthenium red. 243 Mar 46

The role of vasopressin in human hypertension was examined in a series of studies. In patients with primary hyperaldosteronism and benign essential hypertension, circulating vasopressin was generally lower than in normotensive subjects. In contrast, plasma vasopressin was increased (p less than 0.001) in patients with malignant-phase hypertension. However, compared to infused vasopressin in normal subjects, when plasma levels of up to 120 pg/ml did not affect blood pressure, the increased levels found in malignant hypertension could not account for the hypertension. The possibility that there may be an increased pressor sensitivity to vasopressin in hypertension was examined by infusing the peptide into nine patients with essential hypertension. This showed a slight increase in sensitivity compared to normotensive subjects, but again this was insufficient to account for the discrepancy between the circulating level of vasopressin and the extent of the raised blood pressure in the hypertensive patients. The effect of chronically elevated levels of vasopressin was studied in a group of patients with the syndrome of inappropriate ADH excess as a consequence of bronchogenic carcinoma. In spite of having chronically elevated levels of vasopressin, these patients had normal blood pressures for their age and sex. Our results suggest that, although vasopressin is elevated in malignant hypertension, it does not contribute significantly to the raised blood pressure, and its increase is probably a consequence of volume shrinkage through renal salt and water loss.
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PMID:Vasopressin and hypertension in man. 243 62

The mechanism of ion transport across principal cells of rat cortical collecting tubules (CCT) and its regulation by vasopressin (ADH) has been studied in the isolated perfused tubule. To amplify the response to ADH rats were treated with 5 mg I. M. desoxycorticosterone 4-9 days prior to the experiments. Addition of 2 X 10(-10) mol X l-1 ADH increased the transepithelial voltage from -5.1 +/- 0.7 mV to -16.1 +/- 1.4 mV (n = 37) and decreased the transepithelial resistance from 51 +/- 4 omega cm2 to 39 +/- 2 omega cm2 (n = 33). Optical and functional differentiation of impalements of principal and intercalated cells was made and only data of principal cells are presented. ADH depolarized the apical membrane from 79 +/- 1 mV to 66 +/- 2 mV (n = 26) and decreased the fractional resistance of the apical membrane from 0.76 +/- 0.04 to 0.70 +/- 0.04 (n = 13). These ADH effects were prevented by 10(-5) or 10(-4) mol X l-1 luminal amiloride which hyperpolarized the apical membrane when added in the presence or absence of ADH. Apical and basolateral membranes were dominated by large K+ conductances and addition of 3 mmol X l-1 barium to bath or lumen perfusates increased transepithelial resistance almost two-fold, whereas luminal amiloride increased the transepithelial resistance only by 26-35%. Ouabain (0.5 mmol X l-1, bath) depolarized the basolateral membrane and decreased its K+ conductance. These effects were prevented by the simultaneous presence of apical amiloride suggesting that the only route of Na+ entry into the principal cells occurred via the amiloride sensitive Na+ conductance. We conclude that ADH stimulates Na+ reabsorption and K+ secretion in the rat CCT primarily by increasing the Na+ conductance in the apical cell membrane.
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PMID:Electrophysiological studies in principal cells of rat cortical collecting tubules. ADH increases the apical membrane Na+-conductance. 244 57

1--The mechanism of the vasopressin-induced, facilitated transport across toad urinary bladder was studied by treating the luminal membrane of the epithelium with the following reagents of protein functional groups: NEM (SH groups), SITS (amino groups), EEDQ (carboxylic groups), DEPC (histidine). 2--Treatment of the luminal side of the epithelium by NEM strongly inhibits the ADH-induced urea transport, leaving unmodified the effect of the hormone on the flux of antipyrine, a lipid soluble molecule. These results confirm the hypothesis that the urea carrier is of proteic nature. 3--Treatment of the luminal side by SITS strongly inhibits ADH action on urea and antipyrine permeability; thus this effect can be considered rather unspecific. 4--On the contrary the EEDQ effect is more specific; in fact treatment of the luminal side by EEDQ strongly inhibits ADH effect on the permeability of urea, slightly increasing the ADH effect on that of antipyrine. 5--Finally, the luminal treatment by diethylpyrocarbonate inhibits almost completely the ADH action on the urea fluxes, slightly increasing the hormone effect on the antipyrine ones. 6--Based on these results we conclude that carboxylic groups and the imidazolic ring are more important than the amino groups in determining the urea transport across toad bladder, in the presence of ADH.
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PMID:Effect of reagents of protein functional groups on the ADH-induced urea facilitated transport across toad urinary bladder. 245 74

Arginine vasopressin (antidiuretic hormone, ADH) stimulation of sodium transport in high electrical resistance epithelia is accompanied by adenylate cyclase stimulation and cAMP accumulation. The hypothesis of direct phosphorylation of the purified amiloride-blockable epithelial Na+ channel protein by cAMP-dependent protein kinase A after ADH treatment of cultured cells was investigated in this study. Phosphate-depleted A6 cells (a cell line derived from toad kidney) were exposed to 32PO4(3-) in the absence or presence of basolateral ADH (100 milliunits/ml). After 20 min (the time needed for ADH to increase maximally Na+ transport), the Na+ channels were extracted from the cells and purified. At every stage of purification, only one subunit of the Na+ channel, namely, the 315-kDa subunit, was specifically phosphorylated as assessed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and autoradiography or scintillation counting. In addition, a polyclonal antibody raised against purified epithelial Na+ channel protein was able to immunoprecipitate the phosphorylated channel protein from a detergent-solubilized fraction of vasopressin-treated A6 cells. This same subunit was also specifically phosphorylated in vitro when the purified Na+ channel protein was incubated with gamma-[32P]ATP and the purified catalytic subunit of the cAMP-dependent protein kinase. Thus, only a single component, the 315-kDa subunit, of the Na+ channel protein complex (which is composed of six subunits) can be phosphorylated both in vivo and in vitro. This subunit is selectively phosphorylated by the catalytic subunit of cAMP-dependent protein kinase to a level of 2-3 mol of 32P/mol of protein.
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PMID:Phosphorylation of a single subunit of the epithelial Na+ channel protein following vasopressin treatment of A6 cells. 245 53

Vasopressin (ADH) acts in humans mainly upon renal collecting tubules. By changing their water permeability it plays a key role in regulation of renal water excretion. Acting upon vascular smooth muscle cells, it causes vasoconstriction and raised arterial blood pressure. This hormone was also proven to cause constriction of cultured mesangial cels, it causes vasoconstriction and raised arterial blood pressure. This urea (Seldin, Giebisch 1985), to release the natriuretic hormone as well as to stimulate hepatic glycogenolysis (Abramov et al. 1987). The influence of vasopressin upon peritoneal transport of solutes was studied, too. ADH influenced the passage of phosphate and rubidium through the isolated rabbit mesentery (Berndt, Gosselin 1961) as well as sodium flux through isolated rabbit omentum (Shear et al. 1966). It caused the drop in urea dialysance in dogs subjected to peritoneal dialysis (Henderson et al. 1971). The subject of our study was the assessment of the action of the antidiuretic hormone under "in vitro" conditions upon the peritoneal transfer of urea, the solute present in human body fluids and removable by peritoneal dialysis.
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PMID:Vasopressin-induced changes in permeability of peritoneal mesothelium for urea "in vitro". 248 58

Six new cases of psychogenic water intoxication are discussed in the light of 150 observations published in the literature since 1935. 87% of all patients were schizophrenic, and 13% had other psychoses and a variety of functional and organic psychopathies. Psychogenic polydipsia is a prerequisite of psychogenic water intoxication. Water intake either overrides an intact osmoregulation (46% of all cases) or, allied to an inadequate urinary dilutional capacity (54%), leads to a transitory, sometimes repeated, and (in 8% of all cases) lethal water intoxication and hypoosmolality. - The consequence of hypoosmolality is metabolic encephalopathy, with agitation, convulsions and coma as its most common symptoms. Profuse diuresis, enuresis and urinary retention, gastric dilatation, watery vomiting and watery diarrhea are diagnostically helpful symptoms of polydipsia typically denied by the patients. Hypoosmolality/hyponatremia are the hallmarks of water intoxication. However, fewer than 50% of all patients present with the expected maximal urinary dilution. Inadequate ADH activity and increased sensitivity of the renal tubule to antidiuretic hormone are the pathogenetic factors in this inappropriate urinary dilution, while psychosis, psychotropic drugs, diuretics, nicotine and alcohol withdrawal are possible causes and cofactors of polydipsia and inadequate urinary dilution. New aspects of treatment are discussed.
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PMID:[Psychogenic water intoxication]. 264 58

The effects of the absence of various hormones (antidiuretic hormone, thyroid hormone, parathyroid hormone, and calcitonin) on proximal and distal structures were studied in diabetes insipidus (DI) Brattleboro rats. The cross-sectional area of the first segment of proximal convoluted tubules (S1) was significantly reduced in thyroparathyroidectomized (TPTX) DI rats compared with Long-Evans rats (the strain of origin of DI rats) and untreated DI rats. Administration of triiodothyronine (T3, 10 micrograms/day for 7 days) to TPTX-DI rats restored the proximal tubule structure. In the distal convoluted tubule (DCT) the cross-sectional area of the epithelium and the number of nuclei per cross-sectional area were significantly greater in untreated ADH-deficient DI rats than in the control Long-Evans rats. Daily administration of 1-desamino-8-D-arginine vasopressin (dDAVP, 500 ng/day for 3 wk) significantly reduced the size and the number of DCT cells in DI rats. Cortical micropuncture data indicated that the Na+ concentration in the fluid delivered to the DCT and the absolute amount of Na+ reabsorbed along the DCT were higher in DI than in dDAVP-treated DI rats. It is concluded that functional changes in the PCT, subsequent to chronic TPTX, are accompanied by marked alteration of the cell anatomy of this nephron segment, and that the processes that modify the Na load delivered to the DCT and the Na transport in the DCT are accompanied by structural modifications of this segment.
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PMID:A structural study of the rat proximal and distal nephron: effect of peptide and thyroid hormones. 271 59


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