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)

Tubular sodium handling in humans undergoing hypotonic expansion due to the administration of antidiuretic hormone was studied using the clearance of lithium as an index of distal filtrate and sodium delivery. Clearance studies were performed in the morning in eight normal subjects before and on the fourth day of intranasal I-desamino-8-D-arginine vasopressin (dDAVP) administration. Fluid intake was kept constant at 25 ml/kg body weight. After dDAVP body weight increased (2.5 +/- 0.4 kg), plasma sodium fell (from 143 +/- 1 to 128 +/- 5 mmol/liter) and a progressive natriuresis developed. Sodium balance remained negative up to the second clearance study, when the cumulative sodium loss amounted to 148 +/- 96 mmol. Plasma renin activity fell significantly, but plasma aldosterone did not. Inulin clearance rose from 110 +/- 14 to 135 +/- 23 ml/min and lithium clearance from 30.9 +/- 7.6 to 48.9 +/- 15.1 ml/min. Fractional reabsorption of uric acid, phosphate and calcium decreased. Together these changes suggest that the negative sodium balance in hypotonic expansion with dDAVP results from increased filtered sodium load, decreased fractional reabsorption in the proximal tubules, and increased distal delivery. Estimated fractional reabsorption in the distal nephron remained unaltered. The plasma concentration of lithium, of which 10.8 mmol was ingested on the eve of the clearance studies, was not lower during the dDAVP-clearance study. This indicates that the tubular adaptations mentioned are present intermittently, in particular during daytime.
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PMID:Lithium clearance during the paradoxical natriuresis of hypotonic expansion in man. 366 96

Plasma samples obtained at 4-h intervals from goats for at least 24 h before and then during 24 h of deprivation of water were analysed by radioimmunoassay for vasopressin and oxytocin concentrations. The samples were also analysed for osmolality and sodium concentration. The differential effect of night/day versus day/night deprivation was also studied. During the two periods before the two deprivations osmolality varied in a regular manner, with low values occurring at 08.00 h. Sodium concentration followed osmolality, whereas vasopressin did not vary during the period before deprivation. During deprivation vasopressin increased along with osmolality and sodium concentration, with the beginning of the increase occurring after the morning feed. Oxytocin levels did not increase during the period of deprivation. These results do not support the hypothesis of general release of neurohypophysial hormones in response to osmotic stimuli but instead indicate there are species variations with respect to hormonal response to water deprivation.
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PMID:Vasopressin, but not oxytocin, is released in response to water deprivation in conscious goats. 374 67

Cultured A6 epithelial cells from toad kidney form confluent monolayers with tight junctions separating the apical and basolateral membranes. These two membrane domains have distinct compositions and functions. Thus, sodium is actively transported across the epithelia from the apical to basolateral surface via amiloride-inhibitable sodium channels located in the apical membrane. Sodium transport is stimulated by vasopressin, cholera toxin, and 8-bromo-cAMP applied to the basolateral surface where the receptors, adenylate cyclase, and Na+/K+-ATPase are located. In a previous study (Spiegel, S., Blumenthal, R., Fishman, P.H., and Handler, J.S. (1985) Biochim. Biophys. Acta 821, 310-318), we demonstrated that exogenous gangliosides inserted into the apical membrane of A6 epithelia do not redistribute to the basolateral membrane. With the ability to vary selectively the ganglioside composition of the apical membrane, we examined the effects of gangliosides on sodium transport in A6 epithelia. When the apical surface of A6 epithelia were exposed to exogenous gangliosides, sodium transport in response to vasopressin, cholera toxin, and 8-bromo-cAMP was enhanced compared to epithelia not exposed to gangliosides. The effect was observed with bovine brain gangliosides, NeuAc alpha 2----3Gal beta 1----3GalNAc beta 1----4[NeuAc alpha 2----3]Gal beta 1----4Glc beta 1----Cer (GD1a) and Gal beta-1----3GalNAc beta 1----4[NeuAc alpha 2----3]Gal beta 1----4Glc beta 1----Cer (GM1), but not with the less complex ganglioside, Neu-Ac alpha 2----3Gal beta 1----4Glc beta 1----Cer (GM3). We examined A6 cells for endogenous gangliosides and found that, whereas GM3 was a major ganglioside, only trace amounts of GM1 and GD1a were present. Based on cell surface and metabolic labeling studies, these gangliosides were synthesized by the cells and were present on the apical as well as the basolateral surface. Bacterial sialidase, which hydrolyzes more complex gangliosides to GM1, was used to modify the endogenous gangliosides on the apical surface; after sialidase treatment, the epithelia were more responsive to vasopressin, cholera toxin, and 8-bromo-cAMP. Thus, gangliosides may be modulators of sodium channels present in the apical membrane of epithelial cells.
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PMID:Gangliosides modulate sodium transport in cultured toad kidney epithelia. 378 88

After alterations in sodium balance, osmotic reactivity of vasopressin (AVP) release was evaluated in seven conscious dogs during bilateral intracarotid infusions of hypertonic saline. A low-sodium diet reduced plasma sodium concentration by 3%; deoxycorticosterone acetate (30 mg/day for 2 days) elevated the concentration by 1%. Neither treatment altered resting plasma AVP. Hypertonic intracarotid infusions increased jugular plasma osmolality by 20 +/- 2 mosmol/kg independent of manipulations. Plasma AVP values were significantly increased (P less than 0.05) in sodium-depleted dogs compared with values of the control animals. In addition, the osmotic reactivity of AVP release was evaluated during exogenous administration of angiotensin II (ANG II). Intravenous infusion of ANG II (5 ng . kg-1 . min-1) increased plasma concentration of ANG II but did not alter concentration of plasma AVP. The slope for the relationship of jugular plasma osmolality to plasma AVP during hypertonic intracarotid infusions was significantly increased with intravenous infusion of ANG II. Sodium depletion and intravenous ANG II potentiate the relationship of plasma osmolality and plasma AVP when evaluated with intracarotid hypertonic saline infusions in dogs.
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PMID:Effects of sodium depletion and angiotensin II on osmotic regulation of vasopressin. 394 42

We evaluated the effects of human calcitonin (hCT) on electrolyte excretion in hormone-deprived rats, that is, in the absence of endogenous parathyroid hormone, antidiuretic hormone, thyrocalcitonin and glucagon, the effects of which might have interfered with those of exogenous calcitonin. Plasma hCT levels, measured by radioimmunoassay, varied from 0 to 32 ng/ml. In these rats, hCT decreased magnesium (Mg) and calcium (Ca) excretion in a dose-dependent fashion. Maximal decreases were observed for hCT plasma concentrations comprised between 3 and 5 ng/ml, and persisted at the highest doses. Sodium, potassium, water, and total solute excretions were constant in the calcitonin concentration range explored. The same was observed for phosphate, except that slight but significant phosphaturia was elicited by the highest doses. Calcium and phosphate infusions to attenuate the fall in plasma Ca and phosphate concentration subsequent to hCT infusion, did not alter the hormonal effect on Ca and Mg excretion. hCT can therefore directly modulate Mg and Ca reabsorption by the kidney at plasma concentrations within the physiological range. The maximal effects on Mg and Ca reabsorption were obtained at plasma concentrations which are generally reached after maximal stimulation of endogenous calcitonin secretion. It is suggested that in rats, endogenous secretion of calcitonin stimulates Ca and Mg renal reabsorption without modification of sodium and phosphate excretion.
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PMID:Modulation by calcitonin of magnesium and calcium urinary excretion in the rat. 399 91

1. The capacity of adaptation of toads (Bufo bufo) to environments of high salinity was studied and the relative importance of skin, kidney and urinary bladder in controlling the balance of water and salt was assessed.2. Toads were kept in NaCl solutions of 20, 50, 110, 150 and 220 mM and studied in their fourth week of adaptation. A group of animals considered as ;control' was kept in wet soil with free access to water. Plasma, ureter urine, and bladder and colon contents were analysed for sodium, potassium, chloride and osmolality, and total body sodium and water were determined. Absorption of water and (22)Na through the skin, and water flow and sodium excretion through the ureter, of intact animals was studied. Hydrosmotic water transport through the isolated urinary bladder of ;control' and adapted animals was determined. The effects of pitressin and aldosterone on the water and sodium balance are described.3. The survival rates of toads kept in saline concentrations up to 150 mM were identical to that of ;control' animals, but half of the animals kept in 220 mM died within 4 weeks.4. There is a linear correlation between the sodium concentrations and osmolality of plasma and of the external media.5. The sodium concentration in colon contents rose with rising external concentrations, up to values higher than the values in plasma.6. Sodium concentrations and osmolalities of ureter and bladder urine increased in adapted animals, the values for bladder urine becoming much higher than those for ureter urine in animals adapted to 110, 150 and 220 mM.7. Total body water, as a percentage of total weight was kept within very narrow limits, although the total body sodium increased with adaptation.8. Absorption of water through the skin for the same osmotic gradients was smaller in adapted than in ;control' animals.9. The ureteral output of water of toads adapted to 110 and 150 mM-NaCl was larger than the water absorption through the skin.10. Skin absorption of sodium was lower in animals adapted to concentrated saline solutions than in ;control' animals.11. Sodium output by the ureter was identical to skin absorption in ;control' animals adapted to 20, 50 and 110 mM-NaCl but was higher in animals adapted to 150 mM-NaCl.12. Aldosterone increased the absorption of sodium in ;control' and adapted toads, but at all dose levels absorption by control was greater than by adapted animals.13. The stimulation of water absorption by vasopressin in vivo or in isolated bladders was not modified in animals adapted to high salinities.
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PMID:Salt adaptation in Bufo bufo. 463 11

Sodium excretion was studied following experimental elevation of cerebrospinal fluid (CSF) sodium in heterozygous and homozygous (DI) Brattleboro rats given exogeneous antidiuretic hormone. Sodium excretion increased 4.5-fold in heterozygous and 3.5-fold in DI rats. The natriuresis in both groups was rapid in onset and occurred with a simultaneous kaliuresis. Blood pressure increased approximately 10 mmHg in the heterozygous but not in the DI rats. Accordingly, increased blood pressure may contribute to the natriuresis but is not the sole mechanism. Plasma renin concentration did not change in the DI rats during high Na CSF infusion, and chronic bilateral renal denervation did not abolish the natriuresis. Glomerular filtration rate increased during the high Na period in both the intact and renally denervated rats. These data provide evidence that a natriuretic mechanism exists that is not mediated by changes in antidiuretic hormone, renal nerve activity, mean arterial pressure, aldosterone, or angiotensin II, and thus may be due to another circulating substance or natriuretic hormone. This hormone may act totally or in part by increasing glomerular filtration rate.
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PMID:CNS-induced natriuresis and renal hemodynamics in conscious rats. 636 31

The response to an osmolar load (750 ml 2.5% NaCl solution iv preceded by 500 ml water by mouth) was studied in 20 patients with Sheehan's syndrome and 12 normal women. Sodium and osmolality were determined in plasma and urine and arginine-vasopressin (AVP) was measured by RIA in urine. The test was performed in each patient when untreated (group P), after hydrocortisone replacement alone (group F), and combined hydrocortisone and thyroid hormone replacement (group F+T). After the osmolar loading, maximum urinary osmolality in the patients was lower than in the normal women and remained unaffected by both hydrocortisone alone and hydrocortisone and thyroid hormone. Comparison of the mean hourly urinary volume before and after NaCl infusion demonstrated an increase in group P, a decrease in group C, and no change in groups F and F+T. Although free water clearance became negative in all groups, values in groups P, F, and F+T were constantly above that of group C. None of the patients in groups P and F had a significant rise in urine AVP excretion during or after NaCl infusion. Those in group F+T had a slight AVP response which was less than in normal women. Impaired response of AVP to an osmolar load appears to be a constant feature of Sheehan's syndrome even without overt diabetes insipidus.
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PMID:Arginine-vasopressin in postpartum panhypopituitarism: urinary excretion and kidney response to osmolar load. 669 47

The carbon dioxide produced by toad urinary bladders bathed on their mucosal surfaces by sodium Ringer solution and on their serosal surfaces by modified Leibovitz tissue culture medium was analysed by multiple regression on both sodium transport and time. The fractions contributed by metabolism related to transport and by basal metabolism were assessed, and the extent to which these might vary with time was determined. This analytical method, which improves the accuracy with which suprabasal metabolism is estimated, was used to examine the effects on metabolism of vasopressin, aldosterone, and mucosa-positive voltage-clamping. Vasopressin (0.05 u./ml), which on average increased sodium transport 2.9 times and concurrently increased the rate of carbon dioxide production in these transporting tissues, also altered the carbon dioxide production of non-transporting, amiloride-treated control hemibladders. For each hemibladder the ratio of sodium transported to suprabasal carbon dioxide produced after vasopressin was compared with that observed before vasopressin. Differences between the ratios were much reduced when the carbon dioxide productions of the paired transporting hemibladders were corrected for the effects of vasopressin on basal carbon dioxide production. With such analysis, it was confirmed that vasopressin did not alter the stoichiometry of sodium transport. A 30 mV, mucosa-positive voltage clamp, applied near the peak of the response to vasopressin, further increased both sodium transport and carbon dioxide production. No alterations of the ratio of sodium to suprabasal carbon dioxide were seen under these conditions where the maximal rate of active sodium transport in this tissue must have been approached. Active sodium transport was more than doubled some 4 h after adding aldosterone (10(-7) M). However, the related increase in suprabasal carbon dioxide production was greater than threefold. Therefore, whereas the stimulation resulting from vasopressin and voltage clamping had no effect on the ratio of sodium transported to suprabasal carbon dioxide produced, this ratio was reduced significantly by aldosterone. When the sodium transport of aldosterone-treated bladders was increased further by voltage clamping, the ratio of sodium transported to suprabasal carbon dioxide production remained at the reduced value. Sodium transport was increased by approximately 35% more when aldosterone-treated hemibladders were voltage clamped after vasopressin, the control paired hemibladders being exposed to vasopressin and voltage clamping alone.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of hormonal and electrical stimulation of sodium transport on metabolism of toad urinary bladder. 669 80

Animal and human studies demonstrate the dependence of renal prostaglandin (PG) production on dietary sodium chloride intake. The effect of 5 days' low salt diet (10 mmol Na/day plus 0.5 mg/kg Furanthril daily), and 5 days' high salt diet (250 mmol Na/day) on PGE2 and PGF2 alpha plasma levels and their excretion, on plasma renin activity (PRA) aldosterone (A) and vasopressin (VP) was evaluated on 30 normal subjects. Sodium restriction significantly increased plasma PGE2 and PGF2 alpha and their excretion in the urine. High salt intake reduced renal PG production to normal levels. Under low salt conditions PRA and A increased significantly and fell to normal values on high salt regimen. A negative correlation between renal PG production and VP plasma levels and excretion was demonstrated during the changes of dietary sodium intake.
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PMID:Humoral factors involved in the regulation of sodium-fluid balance in normal man. I. Effect of dietary sodium chloride intake on renal prostaglandins, vasopressin and renin-angiotensin-aldosterone system. 674 63


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