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)

1. Acute chloride depletion, without sodium depletion, was produced in rats by a single exchange peritoneal dialysis against sodium bicarbonate solution. Blood volume was restored after dialysis by infusion of salt-free albumin, and exogenous deoxycorticosterone and antidiuretic hormone were given. 2. Clearance studies in the period (3 h) after dialysis revealed no difference in the glomerular filtration rate or in the filtered sodium load between experimental and control rats but urinary sodium concentrations and absolute and fractional sodium excretion were significantly higher in the chloride-depleted group. 3. There was also a significant kaliuresis, increased urinary flow rate and diminished free water reabsorption. Urinary bicarbonate excretion increased to a variable degree but the major rise in anion excretion was 'unmeasured' (Na+ + K+ - [Cl- + HCO3- + PO4(3-)]). 4. It is postulated that chloride depletion imposes limitations on sodium reabsorption in the ascending limb of the loop of Henle.
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PMID:Natriuresis in rats acutely depleted of chloride. 60 61

Fetal growth in utero demands a continuous flow of water and solutes across the placental barrier. We investigated the membrane parameters that control the influx of solutes that are not actively transported and the influx of water. The osmotic conductivity, and the Na+ and Cl- permeabilities of the membrane were measured in chronically instrumented fetal sheep. Transplacental salt flow and water flow were augmented by drainage of fetal urine to the exterior over extended periods of time. Calculation showed that the membrane parameters are: deltaNaCl = 0.83, P.SNaCl = 8.0 10-3 ml.sec-1 kg-1, and LPS = 4.7 10-8 cm5.dyne-1.sec-1.kg-1 (placental surface area S being expressed per kg fetal weight). The chronic infusion of vasopressin into the fetuses at 8 to 11 units per day per kg fetal weight reduced the reflection coefficient deltaNaCl to a mean of 0.63 (P less than 0.03). We concluded that the characteristics of the influx of NaCl and water are compatible with those of a diffusion filtration process, that fetal growth is constrained by the diffusional permeability of the placenta for inert electrolyte and that in the long run fetal growth can only accelerate because placental electrolyte permeability increases. Vasopressin appears to reduce the salt reflection coefficient of the placenta thus enabling the fetus to exert some short term control over its acquisition of water and electrolyte.
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PMID:Fetal homeostasis in relation to placental water exchange. 61 9

Post-traumatic diabetes insipidus was observed in 14 among 702 patients with severe trauma. The cause of the abnormal vasopressin secretion may be cerebral oedema, cerebral contusion near the hypothalamus, pull on the hypophyseal stalk by displacement or gross destruction of the brainstem. The hormonal hypofunction disappears once the cerebral damage has regressed. Treatment consists of exact balancing of water and electrolyte loss, using salt-free solutions. Drug treatment with vasopressin and with ADH-secretion stimulators has given unsatisfactory results, but should be used. Seven of the 14 patients died of their injuries. The symptoms of the diabetes insipidus syndrome regressed in the survivors.
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PMID:[Post-traumatic diabetes insipidus syndrome (author's transl)]. 62 50

The water metabolism was studied in homo- and heterozygous Brattleboro rats suffering from hereditary hypothalamic diabetes insipidus. In homozygous Brattleboro rats the spontaneous water intake and urinary output and the diuretic reactions signficantly increased after water and salt loading. No antidiuretic activity was found in the urine, posterior pituitary or hypothalamus of these animals, and this state was not affected by hyperosmosis. For the heterozygous rats the spontaneous water intake and urinary output and the diuretic reaction exceed the respective control values, the posterior pituitary, the hypothalamus and the urine are of reduced antidiuretic activity and this activity is less mobilizable by hyperosmosis. It is concluded that the ADH-reserve deficiency is total in the homozygous Brattleboro rats, and partial in the heterozygotes. As a result of hyperosmosis, the vasopressin release is of a reduced extent, yet detectable in the heterozygotes.
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PMID:The ADH-reserve capacity in Brattleboro rats. 74 41

1. Bovine neurophysins were prepared by a modified method, in which a Biogel P-60 column was used. This yielded two neurophysin fractions, the first containing neurophysin I and small quantities of the other neurophysins,the second containing neurophysin II and C, and only traces of neurophysin I. 2. Antibodies against neurophysin I, II and C were prepared by an original method, 5 mug in 100 mul water of each of the two fractions were applied on a gel slab and separated by iso-electric focusing in a pH gradient 4--6. The separated bands were visualized with 8-aniline-1-naphthalene sulfonic acid, magnesium salt and strips respectively containing neurophysin I, II or C were cut out. The neurophysin-containing strips were homogenized in complete Freund's adjuvant and injected into rabbits. 3. The specificity of the antisera were tested by immunocytochemistry and by radioimmunoassay. By this latter method, it was determined that cross-reactivity was less than 1%. The cross-reaction, observed with the immunohistochemical method could be eliminated by differential absorption. 4. It was found that neurophysin C antisera were undistinguishable from the neurophysin II antisera, while showing little cross-reactivity with the neurophysin I antisera. This suggests that in vivo neurophysin C is not a real neurophysin, or at least, that it is very similar to neurophysin II. 5. Highly purified bovic focusing method. By modifying a LKB Uniphor electrophoresis apparatus, the elute the proteins without switching off the voltage. The resolution of the technique is close to that offered by analytical gel iso-electric focusing.
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PMID:Bovine neurophysins I, II and C: new methods for their purification and for the production of specific antibodies. 79 44

The anterior, medial and posterior hypothalamic nuclei in alloxan-diabetic male rats were studied by karyometry. Selective responsiveness of separate nuclei of the medial basal hypothalamus (MBH) and the anterior hypothalamus was revealed. In the MBH cell nuclear-size changes were most prominent in the ventromedial nucleus and less pronounced, but significant, in the arcuate nucleus. In the anterior hypothalamus a significant response was produced by the supraoptic nucleus. The authors do not exclude the possibility that the reaction of the neurosecretory cells of the supraotic nucleus is indirect and reflects disturbed vasopressin balance in alloxan-diabetic rats in response to impairment of water-salt metabolism. The responsiveness of the MBH nuclei is considered as evidence for their involvement, the bentromedial nucleus in particular, in hypothalamic control of the endocrine pancreas. Various means by which insulin-sensitive hypothalamic areas may be implicated in this control are discussed.
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PMID:CNS-endocrine pancreas system. I. The hypothalamus response to insulin deficiency. 79 37

Prolactin appears to play a role in osmoregulation of fishes and birds and a possible contribution of this hormone to the regulation of salt and water excretion in mammals has been suggested as well. The present studies were undertaken to investigate the role of osmotic pressure on the secretion of prolactin and the effect of the hormone on renal water excretion in man. The i.v. administration of synthetic thyrotropin releasing hormone (TRH) (7 mug/kg) to five subjects undergoing a maximal sustained water diuresis increased serum prolactin to supraphysiologic levels in all as mean concentration rose from 30.2 +/- 2.9 to 60.2 +/- 5.0 ng/ml (P less than 0.005). This increase was not associated with either significant alterations in renal hemodynamics or sodium excretion and water excretion. The osmoregulation of prolactin release was then investigated by the oral administration of 20 ml/kg of water to seven subjects in 11 studies. While the water load decreased serum osmolality from 293 +/- 285 +/- 1.5 mOsm/kg H2O (P less than 0.001), there was no significant change in prolactin level, 28+/- 1.8 to 30 +/- 2.4 ng/ml. Serum hypertonicity was achieved in six subjects with the infusion of 5% NaCl which increased serum osmolality from 287 +/- 1.8 to 298 +/- 1.4 mOsm/kg (P less than 0.001). While the hypertonic state caused a marked antidiuresis as urinary osmolality rose from 62 +/- 5.9 to 480 +/- 48 mOsm/kg (P less than 0.001), the concentration of prolactin remained unchanged at 28 ng/ml. We conclude that supraphysiologic levels of prolactin have no antidiuretic properties in a vasopressin-free state and that acute alterations in serum tonicity within the range observed do not affect the release of prolactin in man.
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PMID:Osmotic control of prolactin release and its effect on renal water excretion in man. 82 58

The syndrome of inappropriate secretion of antidiuretic hormone was observed in two patients with cystic fibrosis during acute exacerbation of chronic pulmonary disease. It was diagnosed by the accepted clinical and laboratory criteria and confirmed in one case by values for immunoreactive vasopressin that were inappropriately high for plasma osmolality. The severe hyponatremia was corrected by fluid restriction, alone or combined with intravenous treatment with diuretic and hypertonic saline solution. In addition, there was simultaneous therapy of the pulmonary disease. SIADH thus must be added to salt loss as a cause of hyponatremia in CF, and may be more common than realized in patients with CF and severe pulmonary disease.
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PMID:The syndrome of inappropriate antidiuretic hormone secretion as a cause of hyponatremia in cystic fibrosis. 83 69

In these experiments, two groups of animals were studies to evaluate the effect of altering renal tubular sodium-handling on the excretion of acute HCl load. In group, I, normal salt animals hypotonically expanded with antidiuretic hormone (ADH) (using a protocol known to stimulate aldosterone) presented large amounts of sodium to the distal tubule and excreted an acute HCl load much more efficiently than did animals pretreated with either a normal (NL) or low (LO) salt diet alone. In group II, 24 hr after acid-loading, the plasma bicarbonate concentrations were significantly lower in animals pretreated with sodium restriction plus furosemide (F) than in those maintained on a normal (NL) or high (HI) salt diet alone. Acid excretion was maximized (ADH) when distal sodium avidity was stimulated in the presence of adequate distal sodium delivery and minimized (F) when distal sodium delivery was limited (despite possible augmentation of distal sodium avidity). Alterations in urinary sodium excretion alone (LO, NL, HI) did not affect the rate of acid excretion. These data are compatible with the hypothesis that the excretion of an acute HCl load is mediated by existing levels of distal sodium delivery and distal sodium avidity.
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PMID:Evidence that alterations in distal sodium delivery and distal sodium avidity affect the rate of excretion of an acute HCl load. 84 69

1) Fluid retention and ascites are rarely seen in patients with primary biliary cirrhosis (PBC). In an attempt to clarify this clinical observation, renal handling of sodium, water and divalent ions was studied during extracellular volume expansion (ECVE) and maximal suppression of antidiuretic hormone (ADH) secretion in 5 patients with PBC and 9 normal subjects. 2) Mean fractional excretion of sodium, water, phosphate and calculated fractional distal delivery of sodium were significantly greater in patients with PBC as compared with normal controls. Fractional CH20 for given fractional urine flow was similar in patients with PBC and normals. 3) The data suggest that patients with PBC have a greater diminution of proximal tubular reabsorption of sodium in response to ECVE than controls. This augmented elimination of salt during ECVE in patients with PBC may explain the rarity of ascites and edema in this type of cirrhosis.
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PMID:Renal handling of sodium, water and divalent ions in patients with primary biliary cirrhosis. 89 21


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