title: Role of angiotensin II on dihydrofolate reductase, GTP-cyclohydrolase 1 and nitric oxide synthase expressions in renal ischemia-reperfusion.
abstract: BACKGROUND
  The present study was conducted to investigate the role of renal ischemia-reperfusion (IR) and angiotensin II (ANG II) on mRNA and protein levels of renal dihydrofolate reductase (DHFR), GTP-cyclohydrolase 1 (GTP- CH 1), and endothelial and inducible nitric oxide synthase (eNOS and iNOS, respectively).
  
  
  METHODS
  Male Wistar rats were sham operated or received IR (30 min occlusion, and reperfusion for 1 day). Each group was treated separately with water, angiotensin-converting enzyme inhibitor (ACEI) and ANG II receptor type 1 blocker (ARB) for 1 day before the sham operation or IR, and continuously for 1 day after the operation. The mRNA and protein levels were detected by RT-PCR and Western blot, respectively.
  
  
  RESULTS
  IR decreased DHFR mRNA and protein levels (p < 0.01), both of which were restored by ACEI or ARB, whereas GTP-CH 1 expression was unaltered. IR suppressed eNOS dimer while enhancing the monomer (p < 0.01). IR augmented iNOS mRNA, total iNOS protein and iNOS monomer (all p < 0.01) which were attenuated by ACEI or ARB.
  
  
  CONCLUSIONS
  Our study is the first to demonstrate that the heightened ANG II in IR, via stimulation of ANG II receptor type 1, suppresses DHFR and eNOS dimer, while activating both iNOS mRNA and protein levels.
authors.affiliation: Inter-department of Physiology, Graduate School, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
authors.forename: Yuyen
authors.initials: Y
authors.lastname: Seujange
authors.forename: Somchit
authors.initials: S
authors.lastname: Eiam-Ong
authors.forename: Thaweesak
authors.initials: T
authors.lastname: Tirawatnapong
authors.forename: Somchai
authors.initials: S
authors.lastname: Eiam-Ong
mesh_terms: D000804:Angiotensin II / Q000502:physiology*; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D015153:Blotting, Western; D006136:GTP Cyclohydrolase / Q000032:analysis* / Q000235:genetics; D007668:Kidney / Q000098:blood supply*; D008297:Male; D019001:Nitric Oxide Synthase / Q000032:analysis* / Q000235:genetics; D052247:Nitric Oxide Synthase Type II / Q000032:analysis / Q000235:genetics; D052250:Nitric Oxide Synthase Type III / Q000032:analysis / Q000235:genetics; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000201:enzymology*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013762:Tetrahydrofolate Dehydrogenase / Q000032:analysis* / Q000235:genetics
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D012333:RNA, Messenger; D000804:Angiotensin II; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; D013762:Tetrahydrofolate Dehydrogenase; D006136:GTP Cyclohydrolase