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)

MDCK cells accumulate organic osmolytes in response to hyperosmotic NaCl-supplemented medium. We examined time course and inhibitor sensitivity of myo-inositol, sorbitol, and glycerophosphorylcholine (GPC) accumulation in MDCK cells exposed to hyperosmotic NaCl-, D-glucose-, or mannitol-supplemented media. In NaCl medium, cells preferentially accumulated inositol and GPC. In comparison, in glucose medium cells preferentially accumulated sorbitol and GPC. Inositol demonstrated a late (72-96 h) accumulation in glucose medium, although less than in NaCl medium. Mannitol medium did not significantly stimulate accumulation of any of these three osmolytes at 24 h, suggesting that hyperosmolality alone is not sufficient stimulus for their accumulation in this time frame. GPC accumulation was very rapid in glucose medium, and fell to the level induced by NaCl medium at 96 h (approximately 50 nmol/mg protein). Inositol and sorbitol accumulated more gradually, each reaching greater than 400 nmol/mg protein after 96 h. Sorbitol was still accumulating at 96 h, whereas inositol plateaued at 72-96 h. Phlorizin or sorbinil blocked accumulation of inositol or sorbitol, respectively. Sorbitol and GPC accumulation in glucose medium were partially inhibited in absence of serum or in presence of 1 microM vasopressin. Thus NaCl and glucose appear to stimulate specific cellular mechanisms responsible for accumulation of inositol, sorbitol, and GPC in MDCK cells. This accumulation is also modulated by constituents of serum.
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PMID:Modulation of osmolytes in MDCK cells by solutes, inhibitors, and vasopressin. 222 Nov 3

The composition of the extracellular fluid (ECF) must remain stable for cells to function properly. In normal individuals vasopressin and thirst zealously maintain the total ECF concentration, or osmolality, within a narrow range. Disruption of these regulatory mechanisms or rapid addition of solute to the ECF can lead to hyperosmolality. The serious neurologic symptoms that accompany many forms of hyperosmolality can be explained by understanding the physiologic response of cells to the osmotic stress. This review describes the physiology, pathophysiology, differential diagnosis, and therapy of hyperosmolar states.
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PMID:Hyperosmolar states. 226 81

Fractional excretion of lithium (FELi+) has been proposed as an index of fluid delivery to the distal nephron. The increase in FELi+ after the "loop diuretic" furosemide indicates that this postulate may not be valid unless furosemide acts in the proximal tubules. We studied the effect of furosemide (40 mg iv as bolus, followed by 20 mg/h infusion for 90 min) in eight healthy male subjects during maximal water diuresis. Special care was taken to exactly replace urinary losses. Furosemide greatly increased fractional excretion of sodium, from 1.3 +/- 0.4 to 27.8 +/- 3.9%, and water, from 14.2 +/- 1.7 to 38.2 +/- 3.7% (P less than 0.01). There was a disproportionately large increase in FELi+ from 30.3 +/- 3.0 to 53.7 +/- 2.9% (P less than 0.01), whereas fractional excretion of some other alleged proximal markers increased to a lesser extent. Lysine vasopressin, infused at the end of the experiment (n = 7), caused only a small increase in urine osmolality from 225 +/- 17 to 241 +/- 17 mosmol/kg (P less than 0.01), indicating that medullary hyperosmolality had been largely abolished. The most likely explanation of these results is that furosemide has a moderate action in the proximal tubules, and at the same time inhibits preexistent lithium absorption in Henle's loop. In addition, the large difference between FELi+ and maximal urine flow remaining after furosemide suggests that, despite the decreased medullary osmotic gradient, water backdiffusion is unaltered by furosemide or that lithium concentration in the proximal tubule is changed by furosemide.
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PMID:Does lithium clearance reflect distal delivery in humans? Analysis with furosemide infusion. 233 Sep 75

Anesthetized rats of different strains show a hypotensive response to administration of an antagonist of the V1 receptors for vasopressin [d(CH2)5DAVP]. Such an effect is not seen in conscious, water-replete animals or in Long-Evans rats challenged with a subcutaneous injection of polyethylene glycol (PEG) to cause isosmotic hypovolemia. However, Long-Evans rats experiencing a similar volume reduction due to water deprivation show hyperosmolality and exhibit a small hypotensive response to d(CH2)5DAVP. Inhibition of the renin-angiotensin system following administration of d(CH2)5DAVP causes a greater hypotension in PEG-treated than in water-deprived Long-Evans rats. In both experimental conditions, the fall in blood pressure is greater than when captopril administration precedes that of d(CH2)5DAVP, indicating that prolonged administration of d(CH2)5DAVP may be interfering with mechanisms other than those mediated by peripheral V1 receptors. However, administration of d(CH2)5DAVP and captopril to water-deprived Long-Evans rats rarely causes the profound hypotension seen in water-deprived Brattleboro rats given captopril alone. In some adrenalectomized Wistar rats, following withdrawal of salt supplementation, the hypotensive response to d(CH2)5DAVP is the greatest seen in any experimental model. These results indicate that AVP is overtly involved in the support of blood pressure in various hypotensive states and, more importantly, may be responsible for the maintenance of a "normal" blood pressure in some conditions. However, the involvement of AVP in cardiovascular regulation in the majority of normotensive conditions is intriguingly subtle.
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PMID:Vasopressin and the cardiovascular system: physiology or pharmacology? 243 71

Vasopressin secretion is stimulated by hyperosmolality, hypovolemia, or hypotension and is inhibited by hypoosmolality, hypervolemia, or hypertension. These osmotic and hemodynamic influences are mediated by neuronal afferents that originate in separate osmoreceptors or baroreceptors but ultimately converge to act on the same neurosecretory neurons. Functionally, the two control systems are integrated in such a way that osmoregulation is altered but not disrupted by hemodynamic influences. In patients with uncomplicated essential hypertension, basal as well as osmotically stimulated vasopressin is completely normal. The vasopressin response to an acute reduction in blood pressure is also normal if the values are expressed relative to the change in pressure. However, if the plasma vasopressin response is plotted as a function of absolute blood pressure, the line describing the relationship lies well to the right of normal. Thus, although it is completely intact, the baroregulatory mechanism appears to be reset to a higher level in essential hypertension. These results suggest that increased secretion of vasopressin does not contribute to the genesis or maintenance of uncomplicated, untreated essential hypertension but may antagonize the therapeutic effect of some antihypertensive drugs. If so, antagonists of V1 receptors may be useful as second-line adjunctive therapy for this condition.
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PMID:Osmoregulation and baroregulation of plasma vasopressin in essential hypertension. 243 80

To determine the effect of cortisol on vasopressin responses to hyperosmolality, we infused hypertonic saline (HS) (12 meq/kg NaCl) into nine chronically cannulated fetal sheep ranging from 110 to 132 days of gestation. The experiment was performed twice on each fetus, once during a continuous cortisol infusion and once during a vehicle infusion. Administration of HS resulted in a prompt increase in serum osmolality from 292.1 +/- 1.8 to 310.4 +/- 2.5 mosmol/kg. Decreases were seen in pH, partial pressure of O2, and hematocrit from 7.37 +/- 0.01 to 7.31 +/- 0.01, from 22.5 +/- 1.6 to 20.0 +/- 2.0 mmHg, and from 35.6 +/- 1.7 to 32.6 +/- 1.6, respectively. Mean arterial pressure increased from 41.3 +/- 1.4 to 48.9 +/- 2.0 mmHg (P less than 0.01). Arginine vasopressin (AVP) rose from base line after HS (P = 0.11 vehicle experiments, P = 0.04 cortisol experiments), and AVP responses were greater in the cortisol experiments than in the vehicle experiments (delta AVP = 21.9 +/- 10.9 vs. 3.1 +/- 0.9 pg/ml, P = 0.05). Also there was a correlation noted between differences in AVP response and cortisol levels (P less than 0.04). We conclude that cortisol exerts a positive influence on the AVP response to HS in fetal sheep.
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PMID:Effect of cortisol on vasopressin response to hypertonic saline in fetal sheep. 250 98

A close anatomical relationship between nerve terminals containing neuropeptide Y (NPY) and vasopressin (AVP) has been demonstrated in the hypothalamic paraventricular (PVN) and supraoptic nuclei (SON). Furthermore, injections of NPY into the SON increased plasma concentrations of AVP in the rat. These data suggest a potential involvement of hypothalamic NPY in fluid homeostasis in the rat. Therefore, we have studied the effect of elevated plasma osmolality on the concentration of NPY and AVP in the hypothalamus and neurointermediate lobe (NIL) of the pituitary gland. Furthermore, we measured the concentration of NPY in the AVP-deficient Brattleboro rat, which suffers from diabetes insipidus and hyperosmolality. Salt-loading increased plasma osmolality and the concentration of AVP from 2.0 +/- 0.5 to 4.1 +/- 0.6 pg/ml after 7 days. The concentration of NPY in the NIL doubled after 7 days of salt-loading, from 7.9 +/- 0.6 ng/mg protein to 15.2 +/- 1.4 ng/mg protein, whereas AVP concentrations fell from 2285.7 +/- 210.9 ng/mg protein to 187.5 +/- 2.5 ng/mg protein. AVP concentrations in the ME increased transiently after 2 days of salt-loading and returned to control levels after 7 days. In contrast, NPY concentrations in the ME were unchanged at 2 days and were increased 61% after 7 days. NPY concentrations also were significantly elevated after 7 days of salt-loading in the preoptic area (POA) and mediobasal hypothalamus (MBH). The concentration of NPY in the NIL of the homozygous Brattleboro rat was 2-fold greater than in the heterozygous Brattleboro rat and 4-fold greater than in Sprague-Dawley rats used as controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neuropeptide Y (NPY) and vasopressin (AVP) in the hypothalamo-neurohypophysial axis of salt-loaded or Brattleboro rats. 273 Oct 31

A continuous intravenous infusion of aqueous vasopressin (dosage range, 1.0 to 3.0 mU/kg/h) was administered to two patients (respective ages, 2 weeks and 3 years 1 month) who had postoperative central diabetes insipidus to determine if this mode of therapy is helpful in the very young patient. In both patients the polyuria and serum hyperosmolality were corrected. These findings suggest that an intravenous infusion of aqueous vasopressin can provide satisfactory control of the polyuria and electrolyte disturbances found in young children with acute postoperative central diabetes insipidus.
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PMID:Treatment of the young child with postoperative central diabetes insipidus. 291 92

Lung fluid production in utero, a significant source of amniotic fluid, may be regulated by the fetus in response to environmental stress. We monitored changes of maternal and fetal plasma osmolality, plasma arginine vasopressin level, and fetal lung fluid production in response to mannitol-induced change in maternal osmolality in five chronically catheterized ovine fetuses. Four additional ewes and their fetuses did not receive mannitol and served as controls. Maternal infusion of 20% mannitol resulted in maternal and subsequent fetal hyperosmolality (changing from 303 +/- 2 to 322 +/- 2 mOsm and 300 +/- 5 to 319 +/- 8 mOsm, respectively), Mean fetal lung fluid production significantly decreased (from 2.6 +/- 0.4 to 1.6 +/- 0.4 ml/10 min), whereas lung fluid osmolality significantly increased (from 298 +/- 2 to 303 +/- 3 mOsm) in the study animals. No changes in lung fluid sodium or potassium concentrations were observed in study or control fetuses. Fetal plasma arginine vasopressin level significantly increased in the study fetuses (2.2 +/- 0.3 to 5.3 +/- 1.6 microU/ml), though not in control animals. These results indicate that the fetal lamb responds to increased osmolality by decreasing lung fluid production, and that there is a concomitant increase in lung fluid osmolality. This response appears to be mediated via increased fetal plasma vasopressin levels.
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PMID:Fetal lung fluid response to maternal hyperosmolality. 308 67

Arginine-vasopressin (AVP) has been found to influence brain water. Since AVP is released by hyperosmolality into plasma we determined the role of AVP in controlling cerebrospinal fluid (CSF) pressure. Adult cats were anesthetized with pentobarbital and samples of plasma and cisternal CSF were collected 1 or 2 h before i.v. infusion of 2 g/kg of mannitol and for 2 h afterwards. We found a significant increase in plasma osmolality from 320.0 +/- 1.6 to 331.6 +/- -3.4 mOsm/l (mean +/- S.E.M.), while CSF osmolality was unchanged. Prior to mannitol infusion, AVP was elevated to 105 +/- 19 pg/ml in plasma and to 136 +/- 19 pg/ml (mean +/- S.E.M.) in CSF. After infusion of mannitol AVP levels were unchanged in either plasma or CSF. The reduction of CSF pressure by mannitol is independent of AVP in the anesthetized cat.
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PMID:Mannitol-induced hyperosmolality and cerebrospinal fluid vasopressin in anesthetized cats. 310 58


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