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)

In five healthy subjects inhibition of prostaglandin (PG)-synthesis with indomethacin did not significantly alter glomerular filtration, urinary flow rate or sodium and potassium excretion during control urine collection periods or i.v. hypertonic saline infusion. Saline administration was accompanied by a fall in urinary PGEI-excretion from 0.58 +/- 0.14 to 0.26 +/- 0.09 ng/min (p less than 0.05). While indomethacin had no effect on basal urinary osmolality (Uosm), renal concentrating ability following hypertonic saline or i.v. administration of 100 mU lysine-vasopressin significantly increased in the presence of indomethacin with Uosm rising from 805 +/- 25 to 970 +/- 53 mosm/L (p less than 0.01) and from 839 +/- 47 to 996 +/- 62 mosm/L (p less than 0.01), resp. Since this was not accompanied by respective changes in urinary excretion of cyclic adenosine monophosphate (cAMP) mechanisms other than PG-antagonism of vasopressin, such as decreased medullary washout of solute, may contribute to enhanced renal concentrating ability following inhibition of PG-synthesis with indomethacin.
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PMID:Effects of inhibition of prostaglandin-synthesis on renal electrolyte excretion and concentrating ability in healthy man. 21 3

The possibility of uphill transport of urea from the collecting ducts of sheep fed diets containing 14% protein (HP) and 4.9% protein (LP) was explored by measuring cortex to papilla and urine to papilla gradients of urea during ethacrynic acid diuresis. Clearance studies were done on adult, unanesthetized, hydropenic, vasopressin infused sheep. Saline was given to compensate for urine loss during ethacrynic acid diuresis. Following a period of antidiuresis, ethacrynic acid administration caused and increase in fractional water excretion to 0.33 (HP) and 0.44 (LP), an increase in fractional sodium excretion to 0.28 (HP) and 0.41 (LP), and an average increase in glomerular filtration rate of 14.7%. Fractional potassium excretion showed no consistent change. Renal concentrating ability and medullary sodium accumulation were inhibited. Antidiuretic LP and HP medullary urea accumulation patterns were lost. However, identical but small ascending cortex to papilla urea gradients remained in the LP and HP animals. There was no significant difference between the urea concentration in urine and papilla tissue water. The results fail to provide support for the presence of active urea transport from the collecting ducts of sheep fed high or low protein diets.
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PMID:Urea and sodium in sheep kidneys during ethacrynic acid diuresis. 116 73

The effects of iso-osmolar and hypo-osmolar volume expansion on renal water and sodium excretion were studied in dogs during light chloralose anesthesia. Saline or a hypo-osmolar of glucose and urea was given i.v. (20 ml/kg b.w.t. in 60 min). From the start of this infusion the combined weight of the hydration infusate and the dog was maintained constant by a servo system, which controlled the rate of infusion of a hypo-osmolar solution. Consequently the degree of hydration increased linearly during the infusion period after which it remained constant throughout the experiment. No increase in free water clearance was seen after iso-osmolar volume expansion. The rate of excretion of sodium increased considerably. Hypo-osmolar volume expansion provoked a water diuresis during which the rate of excretion of sodium fell to less than 0.1 mumol/kg b.w.t. min. It is concluded that under the present circumstances infusion of iso-osmolar saline is not associated with a decrease in the rate of secretion of vasopressin.
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PMID:Effects on renal water and sodium excretion of infusions of either iso-osmolar saline or a hypo-osmolar solution of non-electrolytes. 127 14

Salt and water balance within the body is controlled by the hormonal influence of vasopressin. Vasopressin is produced in the hypothalamus, stored and released from the posterior lobe of the pituitary, and travels via the blood to the kidneys to regulate the amount and concentration of urine excreted. Oversecretion or undersecretion of vasopressin, eg, diabetes insipidus (DI) or syndrome of inappropriate secretion of antidiuretic hormone (SIADH) results in an imbalance of the salt-to-water ratio. In children this hormonal imbalance may occur secondary to a suprasellar brain tumor and/or the treatment of such. Approximately 50% to 75% of children with suprasellar tumors will develop permanent DI and the remainder will experience transient postoperative DI or SIADH. Pathophysiology of vasopressin's control on salt and water balance and its relationship to suprasellar brain tumors in children are presented. Nursing assessment and intervention parameters for management of DI and SIADH in children with brain tumors are also discussed.
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PMID:Diabetes insipidus and syndrome of inappropriate secretion of antidiuretic hormone in children with midline suprasellar brain tumors. 193 Aug

The content of synaptophysin, a vesicular integral membrane protein of neurons and endocrine cells, and that of vasopressin was measured in neurohypophyses of rats during chronic osmotic stimulation. The animals received 2% NaCl in their drinking water for up to 4 days. Synaptophysin content of neurohypophyses was determined using quantitative immunoblotting, vasopressin content was measured by radioimmunoassay. Salt loading caused a decrease in the content of vasopressin to about 15% of that of control animals, whether expressed per neurohypophysis or relative to the total tissue protein. In contrast, no change was found in the synaptophysin content. Taken together with published evidence of changes in the relative numbers of the hormone-containing neurosecretory granules (NSGs) and the microvesicles (MVs) under the conditions of chronic osmotic stimulation, these results strongly indicate the surface density of synaptophysin on NSGs to be significantly lower than its surface density on MVs.
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PMID:Chronic osmotic stimulation reduces vasopressin but not synaptophysin content in rat neurohypophysis. 212 60

Saline solutions (NaCl, 2 ml, pH 7.4, 10-598 mosmol/kgH2O) were infused over 4 min in conscious rats, via tail artery catheter or intragastric tube. Intragastric infusions of hyper- and hypotonic solutions caused, within 14.4 +/- 2.2 min, a maximal increase and decrease, respectively, of plasma vasopressin (AVP) relative to time controls (r = 0.97; P less than 0.00001) without affecting systemic plasma osmolality (r = -0.09; P less than 0.92). Mean changes of plasma AVP between 11 and 21 min were also correlated with the osmolality of gastric infusion (r = 0.72; P less than 0.000001), whereas systemic osmolality was unchanged (r = 0.14; P less than 0.42). Systemic infusions caused within 9.0 +/- 2.0 min a maximal change in both plasma AVP (r = 0.82; P less than 0.00001) and systemic osmolality (r = 0.97; P less than 0.00001). However, mean changes of plasma AVP between 11 and 21 min weakly correlated with the osmolality of systemic infusions (r = 0.27; P less than 0.20), although correlations between mean changes of systemic osmolality and the osmolality of systemic infusions were significant (r = 0.72; P less than 0.00001). Lack of correlations with mean arterial pressure and heart rate suggest that hemodynamic changes did not mediate the AVP responses. Pretreatment with atropine methyl bromate (2 mg/kg) abolished the AVP response to gastric but not systemic infusions of hypertonic saline. These results indicate that a splanchnic cholinergic receptor mechanism modulates AVP secretion during a moderate gastric intake of salt or water.
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PMID:Splanchnic control of vasopressin secretion in conscious rats. 214 82

We have investigated the role of endogenous opioid peptides in the release of oxytocin (OT) in response to breast feeding and breast stimulation in humans. Five breast feeding women were studied on two separate occasions within 4 weeks of delivery. Saline or naloxone, 4 mg bolus and 6 mg/h, was administered intravenously, in random order. Blood samples were taken at regular intervals. In the saline-infused group OT rose from a baseline of 1.1 +/- 0.1 pmol/l (mean +/- SEM) to a peak of 7.0 +/- 0.9 after 6 min, and in the naloxone-infused group from 1.0 +/- 0.1 pmol/l to 5.8 +/- 1.3 (P less than 0.05). There were no significant differences between the two groups at any time point. Plasma vasopressin (AVP) did not change. In the second study six women in the luteal phase of the menstrual cycle were investigated on two occasions at least 48 h apart. They were similarly infused with either naloxone or saline in random sequence. A mechanical breast pump provided breast stimulation. In saline-infused women OT levels rose from a baseline of 1.0 +/- 0.1 pmol/l (mean +/- SEM) to a peak of 3.0 +/- 1.1 (P less than 0.05) after 6 min, and in naloxone infused women from 1.1 +/- 0.1 pmol/l to 3.0 +/- 1.4 (NS). There were no differences in OT between the groups. AVP did not change. We conclude that endogenous opioid peptides do not modulate OT release during breast feeding or breast stimulation in women.
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PMID:Effect of naloxone on neurohypophyseal peptide responses to breast feeding and breast stimulation in man. 240 Nov

Using rat renal papillary collecting tubule (RPCT) cells in culture, we examined the interactions of extracellular osmolality, vasopressin-stimulated cAMP, and prostaglandin E2 (PGE2) synthesis. Hypertonic solutions composed of equiosmolar amounts of urea and sodium chloride, 900-2,400 mosM, potentiated the increases of intracellular cAMP after vasopressin stimulation. Sodium chloride, rather than urea, was the important solute. The mechanism of this augmented cAMP response was complex, probably involving increased synthesis, decreased degradation, and reduced efflux of cAMP from the RPCT cells. The potentiating actions of hypertonic sodium chloride were specific for vasopressin-stimulated cAMP and were not observed for forskolin or PGE2-stimulated cAMP. Hypertonic solutions inhibited RPCT cell PGE2 production, and sodium chloride, rather than urea, was again the important solute. The enzymatic site of sodium chloride inhibition of PGE2 synthesis was apparently on the phospholipase enzymes, assessed by calcium ionophore and bradykinin stimulation, and not on cyclooxygenase, measured by arachidonic acid responsiveness. Reductions of osmolality, from 1,800 to 300 mosM, acutely increased PGE2 release, possibly through a calcium-dependent stimulation of phospholipase. We conclude that conditions that prevail in vivo during antidiuresis, namely hypertonicity of the papillary interstitium, may augment vasopressin responsiveness through increments of collecting tubule cAMP and reductions of PGE2 which could, in concert, maximize water reabsorption in the collecting tubule.
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PMID:Osmolality, vasopressin-stimulated cAMP, and PGE2 synthesis in rat collecting tubule cells. 242 57

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

We have investigated the importance of endogenous opioids in the differential control of neurohypophysial peptide secretion. The effect of the opioid antagonist naloxone on the vasopressin and oxytocin responses to insulin-induced hypoglycemia was studied in 14 male subjects. Either saline (N = 8) or naloxone (4 mg bolus + 6 mg/h, N = 6) was infused iv during the study. After 60 min infusion soluble insulin 0.15 U/kg was injected. Naloxone infusion for 60 min did not alter basal plasma AVP or OT levels. Insulin-induced hypoglycemia led to a significant rise in plasma AVP in both saline and naloxone-infused subjects (P less than 0.05), which was maximal 45 min after insulin. There was no significant difference in the plasma AVP response to hypoglycemia between the 2 groups. Saline-infused subjects did not show any change in plasma OT in response to hypoglycemia whilst during concurrent naloxone infusion there was a significant rise in OT from 1.9 +/- 0.4 pmol/l before insulin to 3.2 +/- 1.3 pmol/l at 45 min (P less than 0.05). We conclude that there is opioid-mediated inhibition of OT which prevents its release when AVP is secreted in response to insulin-induced hypoglycemia.
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PMID:Opioid-mediated inhibition of oxytocin during insulin-induced hypoglycemic stimulation of vasopressin in man. 283 96


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