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)

The distribution, blood transport, and metabolic clearance of physiological concentrations of antidiuretic hormone were studied in 10 hydrated normal subjects with radioiodinated arginine vasopressin (125I-AVP). At 37 degrees C no binding of 125I-AVP to plasma proteins could be demonstrated, but some metabolites were associated with plasma proteins. 125I-AVP was rapidly distributed into a space approximating the extracellular fluid volume. Metabolic breakdown products became demonstrable within minutes after injection. The mean metabolic clearance rate of 125I-AVP was 4.1 ml/min/kg and the mean plasma half-life 24.1 min. Renal clearance had a mean value of 80 ml/min and accounted for 27% of the total metabolic clearance. It is concluded that in man antidiuretic hormone circulates as a free (non-protein bound) peptide, diffuses readily into the extracellular fluid space, and is metabolized within minutes. A plasma half-life of 24 min is consistent with the duration of antidiuresis after hormone administration or release.
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PMID:Distribution, blood transport, and degradation of antidiuretic hormone in man. 126 58

Experiments were performed in anesthetized rats to examine the possibility that endothelin (ET) modifies renal epithelial function in addition to its well-established hemodynamic actions. Infusion of ET-3 at rates between 34 and 178 ng.kg-1.min-1 was in many cases followed by a rise in urine flow and a persistent decrease in urine osmolality, whereas glomerular filtration rate (GFR) did not significantly change. The extent of ET-induced diuresis was dependent on the response of GFR: in rats in which ET-3 infusion caused a marked reduction of GFR (greater than 70%) ET-induced diuresis was not seen, even though urine osmolality still fell significantly. From animal to animal, ET-induced changes of urine flow or GFR did not correlate significantly with the rate of ET-3 infusion. ET-1, another ET isopeptide, also produced water diuresis when administered in GFR-neutral doses. Urinary excretion of total solutes and of sodium was not significantly altered by ET-3. Infusion of vasopressin blunted the diuretic effect of ET-3, whereas ET-3-induced water diuresis was not measurably altered by chronic or acute treatment with a converting enzyme inhibitor or by acute inhibition of prostaglandin synthesis. Induction of water diuresis was not secondary to an inhibition of vasopressin secretion since it could be demonstrated in homozygous Brattleboro rats in which antidiuresis was produced by the infusion of vasopressin at a rate of 200 microU.kg-1.min-1. These data suggest that ET may be an inhibitory modulator of the hydrosmotic action of vasopressin at the level of the renal collecting duct.
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PMID:Induction of water diuresis by endothelin in rats. 141 80

Antidiuretic and natriuretic responses were observed following gastric distension in anesthetized, water-loaded rats. An increase of intragastric pressure to 25, 30, 35, and 40 cm H2O of 2-minute duration respectively elicited 11, 35, 45, and 55% inhibition of water diuresis with concomitant, graded increase of sodium excretion by the kidney. These antidiuretic and natriuretic responses to gastric distension persisted and sustained the same intensity after acute bilateral cervical vagotomy, indicating that the sensory input conveyed from the gastric mechanoreceptors to central nervous system during gastric distension should involve afferent fibers other than vagus nerve. Rats with diabetes insipidus (D1) produced by hypothalamic lesions were also tested, but neither antidiuresis nor natriuresis in response to gastric distension was observed in these D1 rats whose neurohypophysis contained little antidiuretic hormone (ADH). In conclusion, gastric distension may induce liberation of ADH and probably other neurohypophysial hormone which affects renal handling of sodium and water in anesthetized, water-loaded rats.
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PMID:Antidiuresis and natriuresis induced by gastric distension in water-loaded rats. 145 73

A 54-year-old schizophrenic patient who presented with hyponatremia and nephrotic-range proteinuria was subsequently discovered to have a gastric adenocarcinoma. Psychogenic water drinking, sodium depletion, and cardiac, adrenal, hepatic, and thyroid disease were excluded as causes of hyponatremia. The serum creatinine concentration was normal, and, although renal biopsy showed changes consistent with immune complex glomerulopathy, proteinuria remitted without treatment. Moderately severe hyponatremia persisted, and the diagnosis of gastric adenocarcinoma was made after the onset of early satiety 1 year later. Surgical exploration at the time of partial gastric resection revealed local metastatic lymph node involvement. Following the patient's uneventful recovery from surgery, studies of osmoregulation of vasopressin release and renal water handling were performed to determine the cause of chronic hyponatremia refractory to sodium chloride administration. Oral water loading studies revealed normal urinary diluting ability and appropriate suppression of plasma vasopressin concentrations. However, hypertonic sodium chloride infusion studies revealed a highly significant correlation between plasma osmolality and plasma vasopressin concentration, and a low osmotic threshold for vasopressin release based on linear regression analysis of the plasma vasopressin response to increasing plasma osmolality. Low osmotic threshold for vasopressin release was confirmed by exponential (log linear) and parabolic methods of data analysis. The findings in these studies are consistent with the typical features of the reset osmostat variant of the syndrome of inappropriate antidiuresis. To our knowledge, this is the first report of the occurrence of this syndrome in association with gastric adenocarcinoma.
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PMID:Chronic hyponatremia due to resetting of the osmostat in a patient with gastric carcinoma. 836 36

Antidiuresis, the recovery of water from the lumen of the renal collecting tubule, is regulated by the hypothalamic release of antidiuretic hormone (ADH), which binds to specific receptors on renal collecting tubule cells, stimulates adenylyl cyclase and promotes the cyclic AMP-mediated incorporation of water pores into the luminal surface of these cells. We report here the isolation of the human ADH receptor gene using a genomic expression cloning approach. The gene was used to clone the complementary DNA from a human renal library. The deduced amino-acid sequence of the receptor yields a hydropathy profile characteristic of receptors with seven putative transmembrane regions. This and the comparison with other cloned receptors indicates that the ADH receptor is a member of the superfamily of G-protein-coupled receptors.
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PMID:Molecular cloning of the receptor for human antidiuretic hormone. 153 49

The hypothesis that potassium depletion (KD) might play a role in stimulating the renal synthesis of prostanoids, and that these materials can contribute to hypokalaemic renal dysfunction, has been tested. Healthy women were studied either in normal potassium balance (N,n = 14), or in experimental KD. KD was induced by low dietary potassium intake (less than or equal to 10 mmol day-1) and natriuretic treatment, associated with replacement of net NaCl and water loss. By using different depletive patterns, two groups with estimated cumulative potassium deficits of 160 +/- 43 mmol (KD1, n = 8) and 198 +/- 22 mmol (KD2, n = 6), respectively, were obtained. Renal function by the clearance (cl.) method and urinary PGE2, 6-keto-PGF1 alpha, TxB2 concentrations by the RIA method were measured during hypotonic polyuria (oral water load) and subsequent moderate antidiuresis induced by the infusion of low-dose lysine-8-vasopressin (LVP). Compared to the N group, only in the KD2 group do glomerular and tubular dysfunctions typical of hypokalaemia and reduced prostanoid excretions (significant for 6-keto-PGF1 alpha and TxB2 but not for PGE2) appear during polyuria besides the significant reductions of plasma potassium concentration, urinary potassium excretion and the significant increase in plasma renin activity. During LVP infusion the urinary prostanoid excretions were all significantly lower in absence of significant differences in urinary flow rate. Concerning its renal effects, LVP lost its ability to reduce the creatinine cl., while expressing a trend towards reduction in fractional chloride excretion. Indomethacin pretreatment restored the LVP effect on creatinine cl. and increased the antichloruretic LVP effect (although not significantly). To the extent that urinary prostanoid excretions reflect their intrarenal synthesis, our data demonstrate that KD inhibits this biosynthesis. A depressed production of prostanoids endowed with vasodilating and chloruretic activity probably played a role in attenuating the renal vascular hyporeactivity and the urinary chloride dispersion induced by KD.
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PMID:Effects of experimental potassium depletion on renal function and urinary prostanoid excretion in normal women during moderate anti-diuresis. 154 Oct 86

The distribution and properties of nonapeptide binding sites in the kidney of the anuran Xenopus laevis were investigated using quantitative in vitro autoradiography. The binding studies were performed with [3H]arginine vasopressin (AVP) as ligand because [125I]arginine vasotocin (AVT) lacks biological activity. Specific binding sites for [3H]AVP are located in the glomeruli of the kidney. [3H]AVP binding results in a steady state of association and dissociation between ligand and binding sites. Scatchard and Hill analyses of saturation experiments showed that [3H]AVP binds to a single class of binding sites with a dissociation constant (Kd) of 430 +/- 109 pM and a maximum binding capacity (Bmax) of 5.306 +/- 1.379 fmol/mm2 (n = 8). Displacement studies demonstrated the same affinity of these [3H]AVP binding sites to [3H]AVP, unlabeled AVP, and AVT, whereas mesotocin possesses only weak affinity. Further nonapeptides like oxytocin and isotocin or the mammalian-specific V1 receptor antagonist [1-beta-mercapto-beta,beta-cyclopentamethylene propionic acid)-2-(O-methyl)-tyrosine)-AVP or the V2 receptor agonist (1-deamino-8-D-arginine)-vasopressin or unrelated peptides did not alter the binding of [3H]AVP. The localization of nonapeptide binding sites in the glomeruli with the same affinity to AVP as to AVT agrees with the finding that AVT causes antidiuresis in Xenopus laevis. An earlier study demonstrated Xenopus laevis interrenal tissue to possess a higher sensitivity for AVT than AVP which points to a nonapeptide receptor with a higher affinity for AVT than AVP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Localization and quantification of nonapeptide binding sites in the kidney of Xenopus laevis: evidence for the existence of two different nonapeptide receptors. 156 20

Plasma renin activity (PRA), urinary excretions of PGE2, 6-keto-PGF1 alpha (6KPGF), TXB2 and renal function were determined in healthy women both in normal potassium balance (N, n = 14) and in experimental potassium depletion (KD). KD was induced by natriuretic treatment--associated to replacement of net NaCl and water losses--in the presence of either normal (congruent to 50 mmol/d) or low (less than or equal to 10 mmol/d) dietary potassium intake. By using different depletive patterns, three groups with estimated cumulative potassium deficit (mean +/- SEM) of 124 +/- 38 (KD0, n = 8), 160 +/- 43 (KD1, n = 8) and 198 +/- 22 mmol (KD2, n = 6), respectively, were obtained. Renal function by the clearance (cl.) method and urinary prostanoid concentrations by the RIA method were estimated during hypotonic polyuria (oral water load) and subsequent moderate antidiuresis induced by a low-dose infusion of lysine-8-vasopressin. 1. In KD0 group the potassium depletive treatment was inefficacious in significantly reducing either the plasma potassium concentration (PK) or the urinary potassium excretion (UKV). The reductions of PK and UKV as well as the enhancement of PRA became significant in KD1 and KD2 groups. 2. The urinary prostanoid excretions were not significantly changed in the KD0 and KD1 groups while in the KD2 group they were reduced, mainly concerning the urinary 6KPGF excretion. 3. Furthermore in the KD2 group, with larger potassium depletion, some of the typical hypokalemic renal dysfunctions appeared. The data suggest that a pathophysiologically critical degree of potassium depletion is associated with an inhibited renal prostanoid synthesis as well as an increased renin secretion.
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PMID:Urinary prostanoid excretion in healthy women with different degrees of induced potassium depletion. 163 Nov 74

There is evidence in the rat that stimulation of renal alpha 2-adrenoceptors modulates vasopressin antidiuretic action and vasopressin-stimulated adenylate cyclase activity. In the present study, we tested the ability of various alpha 2-adrenoceptor agonists to antagonize vasopressin-induced antidiuresis in the conscious hydrated dog and to inhibit vasopressin-induced adenosine 3',5'-cyclic monophosphate (cAMP) generation in rat and dog cortical collecting tubules. Vasopressin infusion (0.01 ng.kg-1.min-1) in five dogs resulted in a decrease in free water clearance from 2.90 +/- 0.42 to -0.34 +/- 0.08 ml/min. The vasopressin receptor antagonist SKF 105494 inhibited this response. Administration of norepinephrine (0.5 microgram.kg-1.min-1) or clonidine (20 micrograms/kg), however, failed to alter the vasopressin-induced antidiuresis. In vitro studies demonstrated that epinephrine caused a dose-dependent reduction in vasopressin-stimulated cAMP levels in cortical collecting tubules from the rat (50% effective concentration 32 nM) but not from the dog. The data indicate that there is a species difference in alpha 2-adrenoceptor modulation of vasopressin action.
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PMID:Modulation of vasopressin antidiuretic action by alpha 2-adrenoceptors is species specific. 165 34

The acute effects of i.v. somatostatin (250 mcg bolus followed by 250 mcg/h continuous infusion for two hours) on renal hemodynamics, renal electrolyte and water handling, and urinary excretion of catecholamines and prostaglandins, as well as on plasma concentrations of arginine vasopressin, atrial natriuretic factor, norepinephrine, epinephrine, dopamine, glucagon, and plasma renin activity were studied in seven normal subjects. Somatostatin decreased effective renal plasma flow and glomerular filtration rate, osmotic and free water clearances, urine volume, and sodium and potassium excretion, while urinary osmolality, fractional excretion of sodium, and phosphate excretion increased significantly. Plasma concentrations of arginine vasopressin, atrial natriuretic factor, norepinephrine, epinephrine, and dopamine remained unchanged, while plasma renin activity (3.0 +/- 0.25 vs 2.4 +/- 0.2 ng AngI/ml/h; p less than 0.01) and glucagon levels (40 +/- 11 vs 20 +/- 16 pg/ml; p less than 0.01) decreased. Urinary excretion of norepinephrine, epinephrine, dopamine, PGE2, and PGF2 alpha was suppressed under somatostatin. A significant positive correlation was found between urinary dopamine and sodium excretion (r = 0.7; p less than 0.001) and urinary prostaglandin E2 and glomerular filtration (r = 0.52; p less than 0.01). Without accompanying changes in plasma osmolality and vasopressin concentration significant antidiuresis occurred, suggesting a direct tubular effect of somatostatin. However, the hormone-induced changes are due mainly to the decrease in renal plasma flow. The results demonstrate that somatostatin at supraphysiological doses exerts significant effects on the kidney.
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PMID:Effect of somatostatin on kidney function and vasoactive hormone systems in health subjects. 168 Nov 32


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