INT84598
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Aquaporin-2 (AQP-2), the major water channel responsible for water balance, has been shown to be regulated by the binding of vasopressin to V(2) vasopressin receptors in the medullary collecting duct. alpha(2)-Adrenoceptor agonists such as clonidine have been associated with an increase in free water clearance that was secondary to an inhibition of the ability of vasopressin to increase cAMP levels in the collecting ducts. | |||||||||||||||
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Aquaporin-2 (AQP-2), the major water channel responsible for water balance, has been shown to be regulated by the binding of vasopressin to V(2) vasopressin receptors in the medullary collecting duct. alpha(2)-Adrenoceptor agonists such as clonidine have been associated with an increase in free water clearance that was secondary to an inhibition of the ability of vasopressin to increase cAMP levels in the collecting ducts. | |||||||||||||||
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As shown in Figure 3, taurine-deficient kidneys showed significantly higher levels of non-glycosylated (25 kD) and glycosylated (30-37 kD) forms of AQP 2 than the control and taurine treated groups, which both showed similar AQP 2 levels. | |||||||||||||||
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Since renal AQP 2 is fundamental to the regulation of urine osmolality [24], we determined protein abundance of the whole kidney procured from control, taurine-deficient and taurine-treated groups that had not been subjected to the IR insult. | |||||||||||||||
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The concentration of AQP2 was not significantly changed during the urine concentrating test in Groups 3 and 4, but increased significantly in the other two groups. | |||||||||||||||
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This phenomenon appeared to be related to decreased responsiveness of the kidney to vasopressin caused by a down regulation of the renal vasopressin 2 receptor and AQP2 abundance [27]. | |||||||||||||||
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In addition, our results are in good accordance with animal experiments, which have demonstrated a vasopressin resistant down regulation in expression of AQP2, when urinary concentrating ability was impaired, i. e. in nephrogenic diabetes insipidus, post-obstructive polyuria, and renal failure [1-3,9]. | |||||||||||||||
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Rapid and segmental specific dysregulation of AQP2, S256-pAQP2 and renal sodium transporters in rats with LPS-induced endotoxaemia. | |||||||||||||||
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We aimed to investigate renal water and sodium excretion and in parallel the segmental regulation of renal AQP2 and major sodium transporters in rats with acute LPS-induced endotoxaemia. | |||||||||||||||
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Rapid and segmental specific dysregulation of AQP2, S256-pAQP2 and renal sodium transporters in rats with LPS-induced endotoxaemia. | |||||||||||||||
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In Group 3 and 4, u-AQP2 was no significantly changed during water deprivation. | |||||||||||||||
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The ability to dilute urine was deteriorated in renal insufficiency, presumably due to both a lack of suppression in AVP during water loading and a defect in the regulatory function of AVP on c-AMP with a secondarily up regulation of AQP2 water channels.
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In addition, urine diluting capacity is reduced in hypothyreoidism and adrenal insufficiency with up regulation of AQP2 [4-6], and urine concentration capacity is reduced in thyrotoxicosis and glucocorticoid excess with down regulation of AQP2 [7,8]. | |||||||||||||||
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METHODS: Time course changes in plasma osmolality, AM, arginine vasopressin (AVP), and urinary aquaporin 2 (AQP2) in 17 patients undergoing abdominal surgery under general anesthesia were examined. | |||||||||||||||
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Multivariate stepwise analysis identified plasma AM as the critical independent factor affecting urinary AQP2/Cr level. | |||||||||||||||
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