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高血压的胎儿编程

Fetal programming of hypertension.

作者信息

Alexander Barbara T

机构信息

Department of Physiology, University of Mississippi Medical Center, 2500 N. State St. Jackson, MS 39216-4505, USA.

出版信息

Am J Physiol Regul Integr Comp Physiol. 2006 Jan;290(1):R1-R10. doi: 10.1152/ajpregu.00417.2005.

Abstract

Numerous epidemiological studies suggest an inverse relationship between low birth weight (LBW) and hypertension, an observation now supported by numerous animal studies. The mechanisms linking LBW and hypertension appear to be multifactorial and involve alterations in the normal regulatory systems and renal functions involved in the long-term control of arterial pressure. Recent studies using animal models of fetal programming suggest that programming during fetal life occurs in response to an adverse fetal environment and results in permanent adaptive responses that lead to structural and physiological alterations and the subsequent development of hypertension. This review summarizes the adaptive responses observed in the different models used to induce a suboptimal fetal environment and discusses insights into the mechanisms mediating the fetal programming of hypertension.

摘要

大量流行病学研究表明,低出生体重(LBW)与高血压之间存在负相关关系,这一观察结果现已得到众多动物研究的支持。低出生体重与高血压之间的联系机制似乎是多因素的,涉及参与动脉血压长期控制的正常调节系统和肾功能的改变。最近使用胎儿编程动物模型的研究表明,胎儿期编程是对不利的胎儿环境做出的反应,会导致永久性的适应性反应,进而引起结构和生理改变以及随后的高血压发展。本综述总结了在用于诱导次优胎儿环境的不同模型中观察到的适应性反应,并讨论了对介导高血压胎儿编程机制的见解。

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