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- W3175395767 abstract "Hypoxia increases expression of Hypoxia Inducible Factor (HIF) which salvages cells from damage. PHD regulates HIF-1a activity during hypoxia or normoxia by mechanisms involving nitric oxide (NO) and heme oxygenase (HO). Increased HIF-1a activity increases sodium (Na) excretion (UNaV) but the ion transport mechanisms involved are not known. Since PHD is expressed predominantly in the medulla, this study tested the hypothesis that PHD is selectively involved in renal sodium transport via Na transporter mechanisms in the medulla. The study evaluated differential sensitivity to the effects of inhibitors of Na transporter mechanisms following PHD inhibition with dimethyloxaloylglycine (DMOG; 15 mg/kg). DMOG increased 24-hr UV (1.6 fold) and UNaV (3.2 fold). Following acute salt (NaCl) load (2.5 ml/100 g BW), DMOG also increased UV (1.95 fold) and UNaV (1.8 fold). Hydrochlorothiazide (HCTZ, 3 mg/kg), an inhibitor of NCC, Furosemide (FUR, 12 mg/kg), an inhibitor of NKCC), or Amiloride (200 □g/kg), an inhibitor of ENaC, elicited Increases in UV and UNaV that were inhibited by DMOG by 40±4, 39±3, or 34±4%, respectively. DMOG also increased kidney perfusion (Laser scan) by 20±3%, shifted the pressure/natriuresis curve leftwards, and increased UNOxV (2.8 fold) but elicited paradoxical reductions in GFR and plasma bilirubin. These data indicated that PHD participates in renal function to affect tubular function via NO production affecting NCC, NKCC, and ENaC ion transporter mechanisms to a similar extent." @default.
- W3175395767 created "2021-07-05" @default.
- W3175395767 creator A5035119790 @default.
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- W3175395767 date "2012-04-01" @default.
- W3175395767 modified "2023-10-16" @default.
- W3175395767 title "Prolyl Hydroxylase Domain (PHD)/Hypoxia" @default.
- W3175395767 doi "https://doi.org/10.1096/fasebj.26.1_supplement.1051.8" @default.
- W3175395767 hasPublicationYear "2012" @default.
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