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- W2290186019 abstract "Experimental evidence demonstrates that Prostaglandin E2 (PGE2) production promotes salt excretion in the renal medulla in a setting of activation of the renin-angiotensin-system (RAS). We hypothesized that cyclooxygenase-2 (COX-2) inhibition in Angiotensin II (Ang II)-induced hypertensive rats causes Na+ retention by altering the expression of the Epithelial Sodium Channel (ENaC). Sham-operated male Sprague-Dawley rats (n=8) were compared to Ang II infused rats (0.4μg/kg/min, n=6) and Ang II infused + COX-2 inhibitor; Celecoxib (30 mg/kg/d, n=6). After 5 days, Na+ excretion was increased in Ang II (1.37 ± 0.19 vs. 0.74 ± 0.03 mEq/day; P<0.05) and Ang II + Celecoxib (1.34 ± 0.14 vs. 0.74 ± 0.03 mEq/day; P<0.05) groups. PGE2 urinary excretion was augmented in Ang II infused rats (1,261 ± 147 vs. 643 ± 31 pg/h; P<0.05), while Celecoxib suppressed this effect (596 ± 39 vs. 643 ± 31 pg/h; P=NS). COX-2 protein abundance was increased in the renal medulla of Ang II and Ang II + Celecoxib groups. The mRNA and protein levels of αENaC subunit were up-regulated in cortex and medulla. No difference in αENaC expression was found between Ang II and Ang II plus Celecoxib groups. These results demonstrate the induction of αENaC expression in Ang II-induced hypertensive rats and suggest that the up-regulation of medullary COX-2 is not involved in ENaC regulation and Na+ handling during chronic RAS activation." @default.
- W2290186019 created "2016-06-24" @default.
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- W2290186019 date "2010-04-01" @default.
- W2290186019 modified "2023-09-26" @default.
- W2290186019 title "Effect of COX‐2 inhibition on sodium excretion and ENaC expression in Angiotensin II induced hypertensive rats" @default.
- W2290186019 doi "https://doi.org/10.1096/fasebj.24.1_supplement.605.12" @default.
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