Hemodynamic parameters during normal and hypertensive pregnancy in rats: Evaluation of renal salt and water transporters

Hemodynamic parameters during normal and hypertensive pregnancy in rats: Evaluation of renal salt and water transporters
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DOI:
10.1080/10641950701825887
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发表时间:
2008-01-01
影响因子:
1.5
通讯作者:
Schor, Nestor
Schor, Nestor
中科院分区:
医学4区
文献类型:
--
作者:
Abreu, N. P.;Barboza Monerat Tardin, Joisse Caria;Schor, Nestor

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目的:确定正常妊娠和高血压妊娠期间观察到的细胞外容量扩张的变化是否与肾转运蛋白 mRNA 表达的变化同时发生。方法:将Wistar大鼠分为四组:对照组(C,n=5);怀孕(P,n = 5); N-omega-硝基-L-精氨酸甲酯(L-NAME;50 mg/kg/d)处理的对照(H,n = 6);和怀孕大鼠(HP,n = 6)。在妊娠第 14 天进行血流动力学研究,此时我们还分析了钠转运蛋白(NHE3、Na/K/2Cl 和 Na/Cl)、钾通道 (ROMK2) 和水通道 (AQP2)。结果:正如预期的那样,P 大鼠表现出高心输出量 (CO) 和正常血压 (BP),而 H 大鼠表现出较低的 CO 和升高的血压。在 HP 组中观察到总血管阻力显着(三倍)增加,每搏输出量减少。一氧化氮(NO)合成抑制导致的高血压会削弱妊娠期间的全身血流动力学适应。与C组大鼠相比,P组大鼠ROMK2 mRNA表达量较低,而AQP2 mRNA表达量较高。 H组中AQP2的表达显着高于C组或HP组。 HP组中BSC和NHE3的表达低于P组。 NO 抑制还引起 HP 中肾转运蛋白的改变。结论:我们的结果表明,肾小管转运蛋白变异可能介导妊娠期间的血流动力学适应,尽管我们不能排除其他因素也介导血流动力学变化的假设。
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.