PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 12897087-0 2003 Up-regulation of organic anion transporter 1 protein is induced by chronic furosemide or hydrochlorothiazide infusion in rat kidney. Hydrochlorothiazide 89-108 solute carrier family 22 member 6 Rattus norvegicus 17-44 12897087-12 2003 CONCLUSION: Chronic furosemide or hydrochlorothiazide infusion caused increases in OAT1 protein abundance in rat kidney. Hydrochlorothiazide 34-53 solute carrier family 22 member 6 Rattus norvegicus 83-87 12897087-11 2003 OAT1 protein abundance in cortical homogenates was also increased by hydrochlorothiazide infusion (181 +/- 25 vs 100 +/- 7%, P < 0.01), whereas Na-K-ATPase alpha1 subunit protein abundance was not affected (105 +/- 4 vs 100 +/- 4%, P = 0.34). Hydrochlorothiazide 69-88 solute carrier family 22 member 6 Rattus norvegicus 0-4 10991988-4 2000 p-[(14)C]Aminohippurate (PAH) uptake by rOAT1-expressing oocytes was inhibited in the presence of a thiazide (chlorothiazide, cyclothiazide, hydrochlorothiazide), a loop diuretic (bumetanide, ethacrynic acid, furosemide), or a carbonic anhydrase inhibitor (acetazolamide, ethoxzolamide, methazolamide). Hydrochlorothiazide 141-160 solute carrier family 22 member 6 Rattus norvegicus 40-45 10991988-8 2000 [(14)C]PAH efflux was significantly enhanced when the rOAT1-expressing oocytes were incubated in the presence of unlabeled PAH, alpha-ketoglutarate, acetazolamide, chlorothiazide, or hydrochlorothiazide. Hydrochlorothiazide 183-202 solute carrier family 22 member 6 Rattus norvegicus 54-59