title: Role of renin-angiotensin system and oxidative status on the maternal cardiovascular regulation in spontaneously hypertensive rats.
abstract: BACKGROUND
  The purpose of this study was to investigate the contribution of renin-angiotensin system (RAS) and oxidative status on the maternal cardiovascular regulation at the end of pregnancy in normotensive and spontaneously hypertensive rats (SHR).
  
  
  METHODS
  Blood pressure (BP), mesenteric arterial bed (MAB) reactivity, mesenteric oxidative damage, protein expression, and antioxidant activities were compared between four groups: SHR (SHR-P) and normotensive Wistar controls (W-P) in the 20th day of pregnancy or age-matched nonpregnant rats (SHR-NP and W-NP).
  
  
  RESULTS
  BP in W-P and SHR-P was reduced at the end of pregnancy. The vasodilator effects of angiotensin II (Ang II) and angiotensin 1-7 (Ang-(1-7)) were higher in SHR-P than in other groups. Endothelial nitric oxide synthase (eNOS) expression was increased in W-P and SHR-P compared to nonpregnant groups. Angiotensin-converting enzyme (ACE) and AT(1) receptor expressions were increased in SHR-NP compared to normotensive groups and pregnancy reduced their expressions in SHR. No difference was observed in AT(2) receptor expression among the groups. ACE2 expression was higher in hypertensive than normotensive groups. The levels of thiobarbituric acid-reactive substances (TBARS) were reduced in pregnant compared to nonpregnant groups. Superoxide dismutase (SOD) activity was reduced in SHR-P compared to SHR-NP. However, pregnancy increased catalase (CAT) and glutathione peroxidase (GPx) activities in normotensive rats and SHR, respectively.
  
  
  CONCLUSIONS
  The results suggest that the reduction of BP to normal values at the end of pregnancy in SHR may be related to an increased NO production and vasorelaxation to Ang II and Ang-(1-7) associated with decreased expression of vascular ACE and AT(1) receptors and oxidative status.
authors.affiliation: Laboratório de Tecnologia em Produção de Fármacos, Centro Universitário Estadual da Zona Oeste, Rio de Janeiro, Brazil.
authors.forename: Dayane T
authors.initials: DT
authors.lastname: Ognibene
authors.forename: Lenize C R M
authors.initials: LC
authors.lastname: Carvalho
authors.forename: Cristiane A
authors.initials: CA
authors.lastname: Costa
authors.forename: Ana Paula M
authors.initials: AP
authors.lastname: Rocha
authors.forename: Roberto S
authors.initials: RS
authors.lastname: de Moura
authors.forename: Angela
authors.initials: A
authors.lastname: Castro Resende
mesh_terms: D000803:Angiotensin I / Q000494:pharmacology; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D005260:Female; D006973:Hypertension / Q000503:physiopathology*; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D010446:Peptide Fragments / Q000494:pharmacology; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism; D011247:Pregnancy / Q000502:physiology*; D011249:Pregnancy Complications, Cardiovascular / Q000503:physiopathology*; D051381:Rats; D011918:Rats, Inbred SHR; D017208:Rats, Wistar; D044140:Receptor, Angiotensin, Type 1 / Q000378:metabolism; D012084:Renin-Angiotensin System / Q000502:physiology*; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D010446:Peptide Fragments; D044140:Receptor, Angiotensin, Type 1; D017392:Thiobarbituric Acid Reactive Substances; D000804:Angiotensin II; D000803:Angiotensin I; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat; D013482:Superoxide Dismutase; D007703:Peptidyl-Dipeptidase A; C118790:angiotensin I (1-7)