title: Hemodynamic parameters during normal and hypertensive pregnancy in rats: evaluation of renal salt and water transporters.
abstract: OBJECTIVE
  To determine whether alterations in extracellular volume expansion observed during normal and hypertensive pregnancy run in parallel to changes in the mRNA expression of renal transporters.
  
  
  METHODS
  Wistar rats were divided into four groups: control (C, n = 5); pregnancy (P, n = 5); N(omega)-nitro-l-arginine methyl ester (L-NAME; 50 mg/kg/d)-treated control (H, n = 6); and pregnant rats (HP, n = 6). Hemodynamic studies were performed on day 14 of pregnancy, at which time we also analyzed of the sodium transporters (NHE3, Na/K/2Cl and Na/Cl), potassium channel (ROMK2) and water channel (AQP2).
  
  
  RESULTS
  As expected, P rats presented high cardiac output (CO) and normal blood pressure (BP), whereas H rats presented lower CO and elevated BP. A significant (threefold) increase in total vascular resistance and a decrease in stroke volume were observed in the HP group. Hypertension resulting from nitric oxide (NO) synthesis inhibition blunted systemic hemodynamic adaptations during pregnancy. Compared with C rats, mRNA expression of ROMK2 in P rats was lower, whereas that of AQP2 was higher. Expression of AQP2 was significantly higher in H than in C or HP groups. Expression of BSC and NHE3 was lower in the HP than in the P group. The NO inhibition also provoked renal transporter alterations in HP.
  
  
  CONCLUSIONS
  Our results suggest that tubule transporter variants may mediate the hemodynamic adaptations seen during pregnancy, although we cannot rule out the hypothesis that other factors are also mediating hemodynamic changes.
authors.affiliation: Nephrology Division, Department of Medicine, Federal University of São Paulo (UNIFESP), São Paolo, Brazil.
authors.forename: Np
authors.initials: N
authors.lastname: Abreu
authors.forename: Joisse Caria Barboza Monerat
authors.initials: JC
authors.lastname: Tardin
authors.forename: Mirian Aparecida
authors.initials: MA
authors.lastname: Boim
authors.forename: Ruy R
authors.initials: RR
authors.lastname: Campos
authors.forename: Cassia T
authors.initials: CT
authors.lastname: Bergamaschi
authors.forename: Nestor
authors.initials: N
authors.lastname: Schor
mesh_terms: D000818:Animals; D051399:Aquaporin 2 / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D015870:Gene Expression; D046110:Hypertension, Pregnancy-Induced / Q000503:physiopathology*; D007473:Ion Channels / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism* / Q000503:physiopathology*; D023421:Models, Animal; D024661:Potassium Channels, Inwardly Rectifying / Q000378:metabolism; D011247:Pregnancy / Q000502:physiology*; D011249:Pregnancy Complications, Cardiovascular / Q000503:physiopathology; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D017208:Rats, Wistar; D049992:Sodium Chloride Symporters / Q000378:metabolism; D000074083:Sodium-Hydrogen Exchanger 3; D017923:Sodium-Hydrogen Exchangers / Q000378:metabolism; D028021:Sodium-Potassium-Chloride Symporters / Q000378:metabolism
chemical_list: D051399:Aquaporin 2; D007473:Ion Channels; C086989:KCNJ1 protein, human; D024661:Potassium Channels, Inwardly Rectifying; D012333:RNA, Messenger; C000613385:SLC9A3 protein, human; C000613387:Slc9a3 protein, rat; D049992:Sodium Chloride Symporters; D000074083:Sodium-Hydrogen Exchanger 3; D017923:Sodium-Hydrogen Exchangers; D028021:Sodium-Potassium-Chloride Symporters