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)

Vasopressin (VP) was administered for 1 h intravenously to hydropenic, anesthetized dogs in doses of 1.0-1.25 mU/kg per min. In 14 experiments, sodium excretion (UNA V) increased from a mean of 13 +/- 5 to a peak of 96 +/- 21 mueq/min 40 min after beginning infusion (P less than .001). Urine flow and potassium excretion increased from 0.18 +/-.04 ml/min and 20 +/- 2 meuq/min to peak values of 0.6 +/- .08 ml/min and 61 +/- 9 mueq/min, respectively (P less than .001), with no significant increase in glomerular filtration rate. No significant changes in UNA V occurred in eight sham control experiments of in six experiments in which VP was given at 75 muU/kf per min. To test the hypothesis that VP might be natriuretic indirectly by releasing a natriuretic substance, plasms ultrafiltrates were tested for toad bladder antinatriferic activity(AA). During steady-state control, AA was -10 +/- 3%. Thirty and sixty minutes after beginning VP, AA increased to -24 +/- 3% (P less than .05) and -26 +/- 2% (P less than .001), respectiviely. No significant change in plasma AA occurred in either sham controls or in animals given the subnatriuretic VP dose. Incubation of plasma with 1,000 muU/ml VP caused no increase in AA. The data show that VP natriuresis is accompanied by an increase in plasms AA. The results suggest that vasopressin natriuresis in hydropenic dogs at least in part to the release of a humoral inhibitor of renal tubular sodium transport.
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PMID:Effect of vasopressin on sodium excretion and plasma antinatriferic activity in the dog. 96 68

Unanesthetized dogs were infused with heterologous (hog) renin at 0.33 Goldblatt U/kg per h for 2 h, once normally hydrated and once after 48 h of dehydration. Dehydration increased the average plasma osmolality from 306 to 322 mosmol/kg, the plasma renin activity (PRA) from 0.5 to 1.4 ng/ml per h, and the plasma antidiuretic hormone (ADH) concentration from 1.7 to 3.7 muU/ml, although the latter was not statistically significant. Renin infusion resulted in approximately the same average PRA, about 10 ng/ml per h, in both states of hydration. Mean arterial blood pressure increased during renin infusion in both states of hydration, although the increase was greater when the dogs were normally hydrated. There was no apparent effect of renin infusion on plasma ADH concentration when the dogs were normally hydrated, but in the dehydrated state renin infusion was accompanied by an increase from 3.7 to 6.3 muU/ml in plasma ADH concentrations after 80 min of infusion. There were no apparent changes in plasma osmolality or sodium or potassium concentrations due to the renin infusions; however, plasma osmolality and potassium concentration decreased during the course of the experiment. The results suggest a possible role for the renin-angiotensin system of renin released by the kidney in the control of ADH during dehydration. The metabolic clearance rate of the hog renin was 37 ml/min-kg.
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PMID:Effect of dehydration on stimulation of ADH release by heterologous renin infusions in conscious dogs. 97 Apr 47

1 The influence of potassium loading on the renal excretion of sodium, potassium and solute during high rate vasopressin administration has been investigated in sheep. 2 Adrenalectomized sheep were infused with 0.43 M KCl at 2 ml/min for 2-2.5 hours. Coincident with the rise in plasma potassium concentration, the urinary excretion of sodium, potassium, solute and water was increased as was the reabsorption of solute-free water. The rates of urinary excretion of sodium and potassium, osmolal clearance (COsm) and solute-free water reabsorption (TcH2O) for the first 50 min of potassium infusion were each found to be linearly related to the plasma potassium concentration. 3 After 50 min an infusion of vasopressin at 1 or 4 mu/min was superimposed on the potassium infusion for a period of 30 minutes. The administration of vasopressin was consistently associated with further augmentation of potassium excretion and clearance, of osmolal clearance and of solute-free water reabsorption to values above those anticipated from the pre-vasopressin regression lines for these parameters. Urinary sodium showed a coincident depression in the rate of excretion and clearance during the same period. 4 Thirty to fifty minutes after the cessation of vasopressin infusion the potassium and sodium excretions had returnied to values which approximated the pre-vasopressin relations between plasma potassium and the urinary excretions of these ions. 5 Both rates of vasopressin infusion were equally effective in increasing the potassium clearance. Any differences in clearance between the two rates of vasopressin administration were not statistically significant. 6 The large increments in potassium excretion (averaging greater than 40%) were interpreted as indicating that, when vasopressin is present at high concentrations, the distal tubule is one site of action of the hormone in the nephron of sheep.
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PMID:The effect of high rates of vasopressin administration on renal potassium and sodium excretion during potassium loading in the sheep. 97 79

The effects of 10 days dehydration and rapid rehydration on the sodium and potassium metabolism in the one-humped camel were examined. The research was carried out during two periods in the summer, a cool and a hot period. In the hot period the effects of dehydration were found to be more severe. The potassium metabolism was more affected than that of the sodium. The concentrations of potassium in the urine declined while those of sodium increased. There were also marked changes in the filtered loads, excreted loads, and reabsorption of the two cations. Following rehydration significant changes in the cation metabolism were recorded within 15-45 min. It is suggested that antidiuretic hormone and not aldosterone caused the changes in the two-cation metabolism.
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PMID:Sodium and potassium metabolism in the dehydrated and rehydrated Bedouin camel. 98 85

The influence of an intravenous infusion of saline on the absorption of water and sodium by the jejunum has been investigated in dogs previously submitted to sodium-rich or poor diets. While the net intestinal transport was reduced in sodium-loaded animals, no response was observed in the sodium-deprived dogs, despite identical changes in arterial pressure, intravascular volume and blood dilution indexes. The intestinal response of sodium-deprived dogs became positive after transplanting to their neck vessels the kidneys removed from sodium-loaded animals, thus demonstrating that the presence in the blood of a humoral message of renal origin is required to permit the inhibition of net transport. The difference of the responses depended on the variations of the mucosa-to-serosa unidirectional flux. The net potassium transport did not change significantly. The experimental conditions made unlikely an interference of mineralocorticosteroids, angiotensin or antidiuretic hormone. The present results suggest that the kidney might modulate sodium transport in the jejunum, and perhaps elsewhere in the body, by the way of an additional endocrine function.
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PMID:Renal control of intestinal sodium and water transport in the dog. 98 18

Changes in the excretion of bicarbonate, sodium and potassium in one kidney after exclusion (complete sudden ligation of renal pedicle) of its partner have been studied in 16 dogs undergoing bicarbonate diuresis. Fluid balance, haematocrit, plasma electrolyte and protein concentrations were maintained constant throughout the experiment. Acute contralateral renal pedicle ligation lead to an immediate increase in bicarbonate as well as water, sodium and potassium excretion by the remaining kidney. The rapid and immediate increase in the fractional and absolute rates of bicarbonate excretion was observed at varying levels of bicarbonate loading, with the greatest response occurring at the highest infusion rate. Sodium, potassium and water excretion also increased in parallel with urinary bicarbonate loss. The increase in bicarbonate exposition, glomerular filtration rate, effective renal plasma flow, aldosterone and vasopressin. In 8 sham-operated animals, no abrupt increase in sodium and bicarbonate excretion occurred despite similar continued infusion of sodium bicarbonate. It was concluded that exclusion of one kidney induces immediate adaptive excretory changes for sodium and bicarbonate in the remaining kidney, and that these changes are not accounted for by any of the known factors normally regulating sodium and bicarbonate excretion.
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PMID:Compensatory adaptation of bicarbonate excretion following acute contralateral kidney exclusion in the dog. 100 48

"Refractory" ascites was drained off by combinations of antialdosterone (spironolactone, canrenone) and pseudoantialdosterone (triamterene, amiloride) drugs inducing as high sodium excretion as 100 mEq per day in two patients with liver cirrhosis kept on a 9 mEq Na diet. Potentiation of the natriuretic effects of the two types of antikaliuretic drugs occurred by real synergism rather than addition. Although natriuretic acitivity showed a typical dose-related pattern, potassium excretion was unpredictable. Significant increase in potassium excretion (reversal of the suppression) occurred when 300 mg triamterene was combined with 200 mg canrenone in one of the two patients and when the dose of spironolactone or canrenone was increased from 200 mg to 600 mg within the combinations with 300 mg triamterene or 20 mg amiloride in the other. Parallel increase in sodium and potassium excretions might be caused by a proximal tubular effect or by inhibition of potassium reabsorption along with sodium in Henle's loop. The vasopressin (DDAVP) refractory distorsion of the relationship between osmolal clearance and free water reabsorpton (induced by pseudo-antialdosterone agents and potentiated by antialdosterone drugs) observed in all the 6 cases of the present patient material favoured the "loop hypothesis".
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PMID:Reversal of the suppressed potassium excretion during treatment with combinations of antikaliuretic drugs (spironolactone, canrenone, triamterene, amiloride) in patients with liver cirrhosis. 100 53

In an attempt to determine whether prostaglandin E2 (PGE2) can act centrally to affect the release of vasopressin (ADH), the ventriculo-cisternal system of anaesthetized dogs was perfused with PGE2. When PGE2 was perfused at a rate of 76-4 ng/min (0-19 ml/min), the plasma ADH concentration was unchanged. However, perfusion of PGE2 at a rate of 152-8 ng/min (0-19 ml/min) resulted in a significant increase in the plasma ADH concentration from the control value of 9-0 +/- 2-2 (S.E.M.) to 18-8 +/- 3-9 muu./ml at 10 min and to 41-0 +/- 16-7 muu./ml at 30 min after the start of the perfusion. There were no changes in arterial blood pressure, rectal temperature, plasma osmolality, and the plasma concentrations of sodium and potassium. In additional experiments, i.v. injection of indomethacin (2 or 20 mg/kg) decreased the plasma ADH concentration by approximately 50%. Although this finding is consistent with a role of PGE2 in the control of ADH release, it could also have been due to the observed increases in arterial blood pressure and effective left atrial pressure. Plasma renin activity was unchanged in the indomethacin experiments. It is concluded that PGE2 can act in the central nervous system to stimulate ADH release.
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PMID:Vasopressin release during ventriculo-cisternal perfusion with prostaglandin E2 in the dog. 100 62

Vasopressin (140 muU/min) was infused intravenously into 12 conscious merino ewes for 2 hr. Urine flow rate and free water clearance were consistently reduced. There was no effect upon renal plasma flow, glomerular filtration rate or the rate of excretion of sodium, potassium, magnesium, chloride or phosphate. Although all animals received 75 mmol calcium chloride into the rumen on the previous day, five commenced the experiment with calcium excretion rates of less than 1 mumol/min. In these, vasopressin further decreased calcium excretion. In seven animals with calcium excretion rates between 2 and 20 mumol/min vasopressin had no effect upon either total calcium or free ionized calcium excretion rate.
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PMID:The effect of vasopressin upon the excretion of calcium by the sheep. 104 55

The effects of ouabain, vasopressin, and furosemide on intracellular concentrations of total sodium([Na]) and potassium [K]), on exchangeable sodium ([Na]) and the sodium transport pool ([Nap]) were investigated in isolated short circuited skins of rana esculenta. Furosemide was added to the epithelial bathing solution, vasopressin and ouabain to the corial bathing solution. Results were compared with the amount of net sodium transport measured by short circuit current (scc). Ouabain reduces scc and increases [Na] and [Na]; [K] is decreased. The administration of vasopressin leads to a sharp increase of scc, combined with an enhancement of of [Na] and [Na]; [K] shows no significant change. [Nap] is significantly increased, too, and approximately to the same amount as [Na]. Furosemide causes an increase of scc, whereas a significant change of [Na], [Na] and [K] could not be detected. On the other hand, [Nap] was enhanced significantly. The results support the hypothesis that furosemide like vasopressin is acting by increasing the entry of sodium into the transport compartment of the active cell layer. The result is an increased transfer of sodium across the skin.
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PMID:Effects of furosemide on sodium content and transport pool in frog skin (Rana esculenta): comparison with vasopressin and ouabain. 108 Dec 3


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