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- W2118614887 abstract "It was hypothesized that cyclooxygenase-2 (COX-2) activity promotes urine concentrating ability through stimulation of vasopressin (AVP) release after water deprivation (WD). COX-2-deficient (COX-2 −/− , C57BL/6) and wild-type (WT) mice were water deprived for 24 h, and water balance, central AVP mRNA and peptide level, AVP plasma concentration, and AVP-regulated renal transport protein abundances were measured. In male COX-2 −/− , basal urine output and water intake were elevated while urine osmolality was decreased compared with WT. Water deprivation resulted in lower urine osmolality, higher plasma osmolality in COX-2 −/− mice irrespective of gender. Hypothalamic AVP mRNA level increased and was unchanged between COX-2 −/− and WT after WD. AVP peptide content was higher in COX-2 −/− compared with WT. At baseline, plasma AVP concentration was elevated in conscious chronically catheterized COX-2 −/− mice, but after WD plasma AVP was unchanged between COX-2 −/− and WT mice (43 ± 11 vs. 70 ± 16 pg/ml). Renal V2 receptor abundance was downregulated in COX-2 −/− mice. Medullary interstitial osmolality increased and did not differ between COX-2 −/− and WT after WD. Aquaporin-2 (AQP2; cortex-outer medulla), AQP3 (all regions), and UT-A1 (inner medulla) protein abundances were elevated in COX-2 −/− at baseline and further increased after WD. COX-2 −/− mice had elevated plasma urea and creatinine and accumulation of small subcapsular glomeruli. In conclusion, hypothalamic COX-2 activity is not necessary for enhanced AVP expression and secretion in response to water deprivation. Renal medullary COX-2 activity negatively regulates AQP2 and -3. The urine concentrating defect in COX-2 −/− is likely caused by developmental glomerular injury and not dysregulation of AVP or collecting duct aquaporins." @default.
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- W2118614887 date "2011-12-01" @default.
- W2118614887 modified "2023-09-27" @default.
- W2118614887 title "COX-2 disruption leads to increased central vasopressin stores and impaired urine concentrating ability in mice" @default.
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- W2118614887 doi "https://doi.org/10.1152/ajprenal.00665.2010" @default.
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