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.
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: Crystal A West; Paul A Welling; David A West; Richard A Coleman; Kit-Yan Cheng; Chao Chen; Thomas D DuBose; Jill W Verlander; Chris Baylis; Michelle L Gumz Journal: Am J Physiol Renal Physiol Date: 2017-10-18