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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Marked elevations in the vasopressin concentrations in human umbilical cord blood have been reported previously (4, 8). This could either be a part of generalized increase in the activity of fetal endocrine system at the time of birth, a phenomenon that has led to the concept of fetal participation in the onset of labor, or simply due to the stress of delivery. The present study is an attempt to examine the later possibility. Plasma vasopressin was determined by radioimmunoassay [9] in separately collected arterial and venous blood from the umbilical cords of 24 babies spontaneously delivered and 14 babies born after Caesarian Section in the absence of labor. Arterial acid-base determinations were done in each case. The Apgar Score was evaluated by one individual. In order to obtain a general idea of circulating concentration of this hormone in the neonatal period, vasopressin concentrations were determined in the systemic venous blood of 12 normal and 10 stressed babies. Vasopressin concentrations in the umbilical arterial blood of babies born after spontaneous delivery were remarkably high, as compared to all the other groups. Despite a wide range, between 5-2200 pg/ml, there was no correlation between the magnitude of vasopressin elevation and the severity of fetal asphyxia (Fig. 1). The present finding in part, confirms and expands previously observed increased vasopressin levels in the cord blood after spontaneous vaginal delivery. In addition, a lack of correlation between fetal asphyxia and the vasopressin levels suggests that these high levels may not be related to this form of stress.
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PMID:High vasopressin concentrations in human umbilical cord blood--lack of correlation with stress. 91 83

The effects of hormone binding on the reversible monomer in equilibrium dimer equilibrium of bovine neurophysins I or II in solution have been studied by sedimentation equilibrium measurements performed in conjunction with equilibrium dialysis experiments. Under normal solution conditions saturating amounts of oxytocin displace the neurophysin dimerization equilibrium toward the associated form of the protein to give a dimeric complex with two oxytocin molecules bound per dimer. Vasopressin exerts different influences on this oligomerization process. At low fractional saturation this ligand exhibits a behavior similar to oxytocin with a higher affinity for the neurophysin dimer than the monomer. But in contrast, at higher fractional saturation, vasopressin strongly displaces the aggregation equilibrium toward a monomeric complex bearing two vasopressin molecules. However, in the presence of a high concentration of LiCl two oxytocin molecules are bound per neurophysin protomer (10,000 daltons). These observations, together with earlier data for vasopressin binding, suggest that each neurophysin molecule possesses two structurally distinct hormone binding sites. These observations can be rationalized in a simple schematic model of hormone binding to neurophysin in which oxytocin favors a dimeric form with one hormone binding site available per 10,000 daltons while vasopressin favors the monomeric form with two hormone binding sites available per 10,000 daltons.
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PMID:Interactions of oxytocin and vasopressin with bovine neurophysins I and II. Effects of hormone binding on the protein quaternary structure: a simple model. 93 15

The effects of 60-min intraarterial infusion of vasopressin (0.005 U per kg-min) and epinephrine (0.05 mu per kg-min) on gastric hemodynamics were studied in anesthetized baboons. Total gastric blood flow was measured electromagnetically and radioactive microspheres (15 +/- 5 mu) with three labels were used to determine regional distribution of gastric blood flow and arteriovenous shunting. Control flow was 55 +/- 8 ml per min, with 77.4 +/- 2.7% of flow going to the gastric mucosa and 1.7 +/- 0.4% of injected spheres appearing in the liver. Epinephrine infusion resulted in a sustained vasoconstriction to 18 +/- 5 ml per min with no autoregulatory escape and no changes in arterial pressure or cardiac output. Vasopressin resulted in a decrease in flow to 14 +/- 3 ml per min with no excape. Whereas cardiac output did not change, there was a singificant hypertensive effect during the vasopressin infusion. There was neither redistribution of flow nor change in arteriovenous shunting with either epinephrine or vasopressin. Transmucosal electrical potential difference was 62 +/- 8 mv and did not change significantly with either infusion.
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PMID:Distribution and arteriovenous shunting of gastric blood flow in the baboon: effect of epinephrine and vasopressin infusions. 93 94

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

Recent studies have shown that chronic hypotonic volume expansion (HVE) induced by administration of vasopressin and water stimulates distal hydrogen ion secretion and thereby (a) permits dogs with HCl-acidosis to restore acid-base equilibrium to normal despite continued acid feeding and (b) permits normal dogs to conserve filtered bicarbonate quantitatively despite the natriuresis induced by water retention. To examine whether these effects of chronic HVE are mediated by augmented mineralocorticoid secretion, urinary and plasma aldosterone levels were monitored during prolonged administration of vasopressin. In HCl-fed animals, the HVE-induced rise in plasma [HCO3] (from 13.8 to 21.3 meq/liter) was associated with a rise in aldosterone excretion from 0.45 to 0.88 mug/day (P less than 0.02). In normal animals, in which plasma [HCO3] remained stable during HVE (21.9 vs. 20.0 meq/liter), aldosterone excretion rose from 0.51 to 2.28 mug/day (P less than 0.02) and plasma aldosterone concentration rose from 8.1 to 39.8 ng/100 ml (P less than 0.01). Vasopressin and water were also administered to adrenalectomized animals maintained on glucocorticoids and a slightly subphysiologic replacement schedule of mineralocorticoids. In the HCl-fed adrenalectomized group, plasma [HCO3], instead of rising to normal, showed no significant change (16.9 vs. 15.0 meq/liter). In the non-HCl-fed adrenalectomized group, plasma [HCO3], rather than remaining stable, fell significantly (20.3 vs 16.5 meq/liter, P less than 0.1). Two conclusions can be drawn from this study: (a) the well-known inhibitory effect of volume expansion on aldosterone secretion can be overridden by a potent stimulatory effect on the adrenal produced by severe chronic hypotonicity, and (b) the response of plasma [HCO3] observed during severe chronic HVE is mediated by augmented mineralocorticoid secretion. These findings, furthermore, offer a possible explanation for the puzzling observation that plasma [HCO3] in patients with the syndrome of inappropriate antidiuretic hormone secretion is maintained at normal levels even in the face of severe hyponatremia.
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PMID:The critical role of the adrenal gland in the renal regulation of acid-base equilibrium during chronic hypotonic expansion. Evidence that chronic hyponatremia is a potent stimulus to aldosterone secretion. 99 40

1. Fatty acid synthesis, measured in the perfused liver of genetically obese (ob/ob) mice with 3H2O or [14C]actate, did not show the inhibition by [8-arginine]vasopressin (antidiuretic hormone) that is observed in livers from normal mice. 2. Hepatic glycogen breakdown in obese mice was stimuulated by vasopressin, but not as extensively as in lean mice. 3. If obese mice received a restricted amount of food, then fatty acid synthesis still did not respond to vasopressin, but glycogen breakdown was fully stimulated. 4. Cholesterol synthesis was not inhibited by vasopressin in livers from obese mice. 5. Vasopressin inhibited fatty acid synthesis in intact lean mice, but not in obese animals. 6. These results suggest that genetic obesity could be due to an inborn error within the mechanisms (other than adenylate cyclase) which mediate responses to extracellular effectors.
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PMID:Resistance to hepatic action of vasopressin in genetically obese (ob/ob) mice. 100 43

Angiotensin produced inhibitory and excitatory responses in guinea pig portal vein and excitatory responses in rabbit and rat portal vein. Vasopressin produced inhibitory responses in guinea pig and rabbit portal vein and excitatory and inhibitory responses in rat portal vein. In guinea pig portal vein, inhibition by angiotensin and vasopressin was associated with an increase in membrane potential which was, on average, smaller than that produced by isoprenaline, and with a suppression of spike discharges. Tachyphylaxis of the responses to angiotensin and vasopressin in portal vein was not observed and their effects were unaffected by tetrodotoxin, atropine and phentolamine plus propranolol.
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PMID:Comparison of the excitatory and inhibitory effects of angiotensin and vasopressin on mammalian portal vein. 101 37

Vasopressin was virtually absent from 5 microdissected hypothalamic areas and from the posterior pituitary glands of homozygous Brattleboro rats. The oxytocin concentration was normal in all these areas except for the arcuate nucleus, where it was absent. These results support the concept that Brattleboro rats have a specific defect in biosynthesis of vasopressin. The significance of the absence of oxytocin from the arcuate nucleus in these rats remains to be determined.
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PMID:Vasopressin and oxytocin content of microdissected hypothalamic areas in rats with hereditary diabetes insipidus. 101 33

An experiment was performed in female rats in order to assess the influence and mechanism underlying the effects of hyperglycemia, hypertonic saline and vasopressin upon the gastric acid secretion and mucosal blood flow (MBF). Infusion of isotonic saline did not alter acid output and gastric clearance of plasma aminopyrine whereas hypertonic solutions (20% glucose or 3% NaCl) significantly increased plasma osmolality and decreased the acid secretion within 30 min and recovered to normal levels after 2 h. Vasopressin also effectively inhibited acid secretion. Both hypertonic solutions and vasopressin decreased the mucosal blood flow. However, the ratio (R) of MBF to gastric secretory rate which is a helpful guide to the mechanism of secretory inhibition did not significantly change in either case. We concluded that all three agents probably had a direct action on secretion rather than decreasing MBF. The mechanism of inhabition of acid secretion and its relationship to MBF was suggested and discussed.
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PMID:Mechanism of inhibition of gastric acid secretion by hypertonic solutions and vasopressin. 103 18

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


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