High-salt diets during pregnancy affected fetal and offspring renal renin-angiotensin system.

High-salt diets during pregnancy affected fetal and offspring renal renin-angiotensin system.
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DOI:
10.1530/joe-13-0139
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发表时间:
2013-07
期刊:
The Journal of endocrinology
影响因子:
--
通讯作者:
Xu Z
Xu Z
中科院分区:
其他
文献类型:
--
作者:
Mao C;Liu R;Bo L;Chen N;Li S;Xia S;Chen J;Li D;Zhang L;Xu Z

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宫内环境与胎儿肾脏发育和产后健康有关。研究了妊娠期高盐饮食对绵羊胎儿和子代肾脏功能和肾素-血管紧张素系统(RAS)的影响。在妊娠中后期分别饲喂高盐饲粮(HSD)和正常盐饲粮(NSD) 2个月。测定胎儿和子代的胎儿肾功能、血浆激素及肾RAS关键因子mRNA和蛋白的表达。HSD组胎儿肾钠排泄量增加,尿量减少。HSD组胎儿血尿素氮升高,肾重:体重比降低。在15天和90日龄的后代中也观察到这一比例的改变。孕妇和胎儿血浆抗利尿激素升高,血浆肾素活性和Ang I水平未发生变化,血浆Ang II水平下降。除肾素外,局部肾RAS的关键成分,包括血管紧张素原、血管紧张素转换酶(ACE)、ACE2、AT1和AT2受体mRNA和蛋白的表达在母体高盐摄入后发生改变。结果表明,妊娠期高盐摄入影响胎儿肾脏发育,与肾脏RAS关键因子的表达改变有关,胎儿起源的一些改变在出生后仍然存在,可能是发生肾脏或心血管疾病的风险。
Intrauterine environments are related to fetal renal development and postnatal health. Influence of salty diets during pregnancy on renal functions and renin–angiotensin system (RAS) was determined in the ovine fetuses and offspring. Pregnant ewes were fed high-salt diet (HSD) or normal-salt diet (NSD) for 2 months during middle-to-late gestation. Fetal renal functions, plasma hormones, and mRNA and protein expressions of the key elements of renal RAS were measured in the fetuses and offspring. Fetal renal excretion of sodium was increased while urine volume decreased in the HSD group. Fetal blood urea nitrogen was increased, while kidney weight:body weight ratio decreased in the HSD group. The altered ratio was also observed in the offspring aged 15 and 90 days. Maternal and fetal plasma antidiuretic hormone was elevated without changes in plasma renin activity and Ang I levels, while plasma Ang II was decreased. The key elements of local renal RAS, including angiotensinogen, angiotensin converting enzyme (ACE), ACE2, AT1, and AT2 receptor expression in both mRNA and protein, except renin, were altered following maternal high salt intake. The results suggest that high intake of salt during pregnancy affected fetal renal development associated with an altered expression of the renal key elements of RAS, some alterations of fetal origins remained after birth as possible risks in developing renal or cardiovascular diseases.