Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Hereditary non-X-linked nephrogenic diabetes insipidus (NDI) is caused by mutations in the aquaporin-2 (AQP2) water channel. In transfected cells, the human disease-causing mutant AQP2-T126M is retained at the endoplasmic reticulum (ER) where it is functional and targetable to the plasma membrane with chemical chaperones. A mouse knock-in model of NDI was generated by targeted gene replacement using a Cre-loxP strategy. Along with T126M, mutations H122S, N124S, and A125T were introduced to preserve the consensus sequence for N-linked glycosylation found in human AQP2. Breeding of heterozygous mice yielded the expected Mendelian distribution with 26 homozygous mutant offspring of 99 live births. The mutant mice appeared normal at 2-3 days after birth but failed to thrive and generally died by day 6 if not given supplemental fluid. Urine/serum analysis showed a urinary concentrating defect with serum hyperosmolality and low urine osmolality that was not increased by a V2 vasopressin agonist. Northern blot analysis showed up-regulated AQP2-T126M transcripts of identical size to wild-type AQP2. Immunoblots showed complex glycosylation of wild-type AQP2 but mainly endoglycosidase H-sensitive core glycosylation of AQP2-T126M indicating ER-retention. Biochemical analysis revealed that the AQP2-T126M protein was resistant to detergent solubilization. Kidneys from mutant mice showed collecting duct dilatation, papillary atrophy, and unexpectedly, some plasma membrane AQP2 staining. The severe phenotype of the AQP2 mutant mice compared with that of mice lacking kidney water channels AQP1, AQP3, and AQP4 indicates a critical role for AQP2 in neonatal renal function in mice. Our results establish a mouse model of human autosomal NDI and provide the first in vivo biochemical data on a disease-causing AQP2 mutant.
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PMID:Neonatal mortality in an aquaporin-2 knock-in mouse model of recessive nephrogenic diabetes insipidus. 1103 38

The magnocellular neurones of the hypothalamo-neurohypophysial system (HNS) play a vital role in the maintenance of body homeostasis by regulating oxytocin (OT) and vasopressin (VP) secretion from the posterior pituitary. During hyperosmolality, OT and VP mRNA levels are known to increase by approximately two-fold, whereas during chronic hypoosmolality, OT and VP mRNA levels decrease to approximately 10-20% of basal levels. In these studies, we evaluated changes in cell size associated with these physiological conditions. Cell and nuclear sizes of neurones in the supraoptic nucleus (SON), the nucleus of the lateral olfactory tract (LOT) and the medial habenular nucleus (MHB) were measured from neurones identified by in situ hybridization histochemistry for beta(III)-tubulin mRNA, and measurements were made from OT and AVP magnocellular neurones in the SON after phenotypic identification by immunohistochemistry. Under hypoosmolar conditions, the cell and nuclear sizes of OT and VP magnocellular neurones decreased to approximately 60% of basal values, whereas cell and nuclear sizes of OT and VP neurones in hyperosmolar rats increased to approximately 170% of basal values. In contrast, neither hyperosmolality, nor hypoosmolality significantly affected cell and nuclear sizes in the LOT and MHB. These results confirm previous studies that showed that magnocellular neurones increase cell size in response to hyperosmolar conditions and, for the first time, demonstrate a marked decrease in cell size in the SON in response to chronic hypoosmolar conditions. These dramatic changes in cell and nuclear size directly parallel changes in OT and VP gene expression in the magnocellular neurones of the SON and, consequently, are consistent with the pronounced bidirectional changes in gene expression and cellular activity found during these osmotic perturbations. Our results therefore support the concept of global alterations in the synthetic activity of magnocellular OT and AVP neurones in response to extracellular osmolality.
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PMID:Chronic hypoosmolality induces a selective decrease in magnocellular neurone soma and nuclear size in the rat hypothalamic supraoptic nucleus. 1112 13

We describe a patient with systemic lupus erythematosus (SLE) with lupus psychosis, who showed prolonged consciousness disturbance due to hyperosmolality. A 51-year-old Japanese woman with SLE was admitted to our hospital for the evaluation and treatment of consciousness disturbance on March 5, 1994. She had not been given prednisolone since 1984, and had been depressive since January 1994. She was diagnosed as active SLE with lupus psychosis due to the presence of thrombocytopenia, proteinuria, positive anti-nuclear antibody (x10,240) as well as the elevation of cerebrospinal fluid (CSF) IL-6 level. A treatment with methylprednisolone (mPL) 100 mg/day was started along with 2 courses of steroid pulse therapy (mPL 1 g/day for 3 consecutive days). She recovered partially from the central nervous system manifestations with a decrease in CSF IL-6 level 2 weeks after this treatment. However, her consciousness level was exacerbated again thereafter. Blood examination disclosed the elevation of plasma osmolality (319 mOsm/kg) with poor responses of plasma antidiuretic hormone (4.6 pg/ml). She died from systemic aspergillosis on April 26, 1994. Pathological examination on autopsy showed no abnormality in hypothalamus and pituitary gland. It is suggested that this patient was complicated with lupus psychosis as well as hyporesponsiveness of osmoreceptor. Rheumatologists should be aware of this complication in patients with CNS lupus as a possible cause for intractable CNS manifestations.
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PMID:[Hyperosmolality in central nervous system lupus as a possible complication that results in prolonged consciousness disturbance]. 1112 64

Hypernatraemia is defined as an increase in extracellular sodium concentration, associated with plasma hyperosmolality and cellular dehydration. It can result from excessive water loss, from an increase in the total sodium content or from both mechanisms. As far as neurosurgical pathology is concerned, hypernatraemia due to excessive water loss may be observed in patients who do not sense thirst or are unable to ingest water. Urinary water loss is seen in diabetes insipidus and osmotic diuresis. Extrarenal water losses from pulmonary origin may be observed in intubated or tracheotomized patients. Hypernatraemia with sodium and water retention may be encountered in patients suffering from Cushing diseases or syndromes, or more frequently in those who are given excessive amounts of sodium (hypertonic saline, sodium salts). Clinical manifestations of hypernatraemia consist of neurologic symptoms related to cellular dehydration; their severity is correlated with the rapidity of the onset of the electrolytic disorder. Depending on the pathophysiological mechanism, treatment of hypernatraemia involves stopping sodium intake, restoring normovolaemia and administering hypotonic fluids. Treatment of diabetes insipidus relies on the administration of the antidiuretic hormone and of drugs that increase its secretion rate or its responsiveness in the kidneys.
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PMID:[Hypernatremia in neurosurgical pathology]. 1127 Feb 43

Arginine vasopressin (AVP) is involved in osmotic regulation in the brain and peripheral tissues. To elucidate the regulatory mechanism that involves AVP release in hyperosmolality, we investigated the regulation of the synthesis and release of AVP in chronic salt-loaded rats. In chronic salt-loaded rats, which were generated by free access to water containing 2% NaCl for 7 days, plasma osmolality was significantly increased compared with control value. When tested, the AVP content was significantly higher in plasma but lower in the pituitary and whole brain (hypothalamus, cortex and striatum) than in control rats. The expression of AVP mRNA in the brain was significantly up-regulated compared with that in control rats. These data lead to the suggestion that hyperosmolality stimulates AVP release from the brain and subsequently induces AVP synthesis in the brain. On the other hand, mRNA levels of vasopressin V1a receptor (V1aR), whose down-regulation is known to be a counteraction to the V1aR activation, was not changed in the brain, suggesting that the AVP seems not to interact with the V1aR in the brain. These results suggest that hyperosmosis promotes the release of AVP into plasma, the subsequent induction of AVP mRNA in the brain and its action on the peripheral tissues.
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PMID:Mechanism of AVP release and synthesis in chronic salt-loaded rats. 1180 1

The choroid plexus plays a pivotal role in the production of cerebrospinal fluid (CSF). Messenger RNA (mRNA) transcripts encoding arginine vasopressin (AVP) and the vasopressin 1b receptor (V(1b)R) are found in various structures of the central nervous system, including the choroid plexus. The present study measured AVP and V(1b)R mRNA production in response to plasma hyperosmolality. Compared to rats maintained on water, 2% salt-drinking rats had increased levels of AVP and V(1b)R mRNAs in the supraoptic (SON) and paraventricular (PVN) nuclei of the hypothalamus and in the choroid plexus. The increase in V(1b)R mRNA in the SON and PVN as a result of plasma hyperosmolality may reflect changes in receptor production that, in turn, have a role in AVP autoregulation of hypothalamic magnocellular neurons. The increase of AVP and V(1b)R mRNAs in the choroid plexus further shows the involvement of AVP in the regulation of brain water content and cerebral edema.
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PMID:Salt-loading increases vasopressin and vasopressin 1b receptor mRNA in the hypothalamus and choroid plexus. 1188 9

Effects of hypobaric hypoxemia on endocrine and renal parameters of body fluid homeostasis were investigated in eight normal men during a sojourn of 8 days at an altitude of 4,559 m. Endocrine and renal responses to an osmotic stimulus (5% hypertonic saline, 3.6 ml/kg over 1 h) were investigated at sea level and on day 6 at altitude. Several days of hypobaric hypoxemia reduced body weight (-2.1 +/- 0.4 kg), increased plasma osmolality (+5.3 +/- 1.4 mosmol/kgH(2)O), elevated blood pressure (+12 +/- 1 mmHg), reduced creatinine clearance (122 +/- 6 to 96 +/- 10 ml/min), inhibited the renin system (19.5 +/- 2.0 to 10.9 +/- 0.9 mU/l) and plasma vasopressin (1.14 +/- 0.16 to 0.38 +/- 0.06 pg/ml), and doubled circulating levels of norepinephrine (103 +/- 16 to 191 +/- 35 pg/ml) and endothelin-1 (3.0 +/- 0.2 to 6.3 +/- 0.6 pg/ml), whereas urodilatin excretion rate decreased from day 2 (all changes P < 0.05 compared with sea level). Plasma arginine vasopressin response and the antidiuretic response to hypertonic saline loading were unchanged, but the natriuretic response was attenuated. In conclusion, chronic hypobaric hypoxemia 1) elevates the set point of plasma osmolality-to-plasma vasopressin relationship, possibly because of concurrent hypertension, thereby causing hypovolemia and hyperosmolality, and 2) blunts the natriuretic response to hypertonic volume expansion, possibly because of elevated circulating levels of norepinephrine and endothelin, reduced urodilatin synthesis, or attenuated inhibition of the renin system.
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PMID:Prolonged hypobaric hypoxemia attenuates vasopressin secretion and renal response to osmostimulation in men. 1196 Sep 41

The aim of this study is to pursue roles of N-methyl-d-aspartate (NMDA) receptors in the anteroventral third ventricular region (AV3V; a pivotal area for autonomic functions) in controlling vasopressin (AVP) release and cardiovascular system. In conscious rats, we examined effects of AV3V infusion of MK-801 (a selective antagonist for NMDA receptor) on plasma AVP, osmolality, electrolytes, arterial pressure and heart rate, in the absence or presence of NMDA, hyperosmotic or prostaglandin (PG) E2 stimulus. The AV3V infusion of NMDA caused significant increases in plasma AVP, osmolality and sodium, hematocrit, arterial pressure and heart rate after 5 or 15min. When NMDA was administered into the cerebral ventricle, relatively smaller elevations were observed only in plasma AVP and arterial pressure. The effects of AV3V infusion of NMDA were nearly completely prevented by MK-801 applied to the same region before 15min. The application of MK-801 was also potent to block rises of plasma AVP elicited by AV3V injection of PGE2 or i.v. infusion of hypertonic saline. However, it inhibited neither increases of arterial pressure and heart rate due to the PGE2 treatment nor those of arterial pressure, plasma osmolality and sodium in response to the osmotic load. Histological analysis on the AV3V infusion sites of NMDA, MK-801 and PGE2 indicated that they had been located in the structures such as the median and medial preoptic nuclei, periventricular nucleus and medial preoptic area. These results suggest that stimulation of AV3V NMDA receptors in the basal state may facilitate AVP secretion and cause pressor and tachycardiac actions, and that these receptors may be involved in both the hyperosmolality- and PGE2-induced hormone release, but not in the cardiovascular responses to these stimuli.
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PMID:Contribution of N-methyl-d-aspartate receptors in the anteroventral third ventricular region to vasopressin secretion, but not to cardiovascular responses provoked by hyperosmolality and prostaglandin E2 in conscious rats. 1212 57

Because the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) can cause neurologic sequelae with the potential to affect long-term outcomes, its prompt recognition and treatment are essential. Normally, antidiuretic hormone (ADH) is secreted when effective circulating blood volume is decreased. SIADH is marked by secretion of ADH in the presence of effective or normal circulating blood volume. This causes plasma hyponatremia simultaneously with plasma hypo-osmolality and inappropriate hyperosmolality of the urine. This article explains the pathophysiology of the syndrome; describes its diagnosis, clinical course, and treatment; and exemplifies the syndrome with a case study.
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PMID:SIADH: a case review. 1214 36

Nephrogenic diabetes insipidus is caused by an inability of the kidney to concentrate urine despite adequate concentration of vasopressin in blood and is characterized by polyuria, polydipsia, and hyposthenuria in the presence of plasma hyperosmolality. Nephrogenic diabetes insipidus is the result of defects in water homeostasis in the kidney. Nephrogenic diabetes insipidus occurs when the kidneys cannot or do not respond to vasopressin. There are 2 categories of nephrogenic diabetes insipidus. Congenital nephrogenic diabetes insipidus is a rare, inherited, irreversible cause of polyuria and polydipsia in humans that is even rarer in animals. Acquired nephrogenic diabetes insipidus is more common and is often secondary to illness or medication that interferes with the action of vasopressin in the renal tubules. Unlike congenital nephrogenic diabetes insipidus, acquired or secondary nephrogenic diabetes insipidus is often reversible with correction of the associated or causative problem.
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PMID:Water transport in the kidney and nephrogenic diabetes insipidus. 1232 98


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