孕期高盐饮食与血管紧张素相关的心脏改变。
High-salt diet during pregnancy and angiotensin-related cardiac changes.
机构信息
Institute for Fetal Origin-Diseases, First Hospital of Soochow University and Perinatal Biology Center, Soochow University, Suzhou, China.
出版信息
J Hypertens. 2010 Jun;28(6):1290-7. doi: 10.1097/HJH.0b013e328337da8f.
OBJECTIVES
High-salt intake has been demonstrated in link to hypertension, and cardiovascular diseases could be programmed in fetal origins. We determined the influence of high-salt diet during pregnancy on the development of the heart.
METHODS
Fetal cardiac structures, cell cycle, renin-angiotensin system (RAS), and epigenetic alternations in the heart following maternal high salt intake during pregnancy were examined.
RESULTS
Following exposure to high salt, disorganized myofibrillae and mitochondria cristae loss were found in the fetus, S-phase for cardiac cells was enhanced, plasma angiotensin II decreased, and cardiac angiotensin II increased in the fetus. Angiotensin II-increased S-phase in the fetal cardiac cells was primarily via AT1 receptor mechanisms. AT2 receptor mRNA and protein in the fetal heart were not affected, whereas AT1 receptor protein, AT1a, and AT1b mRNA were increased. DNA methylation was found at the CpG sites that were related to AT1b receptors in the fetal heart. Cardiac AT1 receptor protein in the adult offspring was also higher following exposure to prenatal high salt.
CONCLUSION
The results suggest a relationship between high-salt diet in pregnancy and developmental changes of the cardiac cells and renin-angiotensin system.
目的
高盐饮食已被证明与高血压有关，心血管疾病可能起源于胎儿期。我们旨在确定孕期高盐饮食对心脏发育的影响。
方法
检测了孕期母体高盐饮食对胎儿心脏结构、细胞周期、肾素-血管紧张素系统（RAS）和心脏表观遗传改变的影响。
结果
暴露于高盐后，胎儿心肌纤维和线粒体嵴出现排列紊乱和缺失，心肌细胞 S 期增加，血浆血管紧张素 II 减少，胎儿心脏血管紧张素 II 增加。胎儿心脏细胞中血管紧张素 II 诱导的 S 期主要通过 AT1 受体机制。胎儿心脏中的 AT2 受体 mRNA 和蛋白不受影响，而 AT1 受体蛋白、AT1a 和 AT1b mRNA 增加。在胎儿心脏中发现与 AT1b 受体相关的 CpG 位点的 DNA 甲基化。在成年子代中，暴露于产前高盐后，心脏 AT1 受体蛋白也增加。
结论
这些结果表明，孕期高盐饮食与心脏细胞和肾素-血管紧张素系统的发育变化有关。
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