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本文引用的文献

1
Nutritional manipulations in the perinatal period program adipose tissue in offspring.围产期的营养干预可调控后代的脂肪组织。
Am J Physiol Endocrinol Metab. 2013 Nov 15;305(10):E1195-207. doi: 10.1152/ajpendo.00231.2013. Epub 2013 Sep 17.
2
Prenatal hypoxia causes long-term alterations in vascular endothelin-1 function in aged male, but not female, offspring.产前低氧可导致老年雄性,而非雌性,子代血管内皮素-1功能长期改变。
Hypertension. 2013 Oct;62(4):753-8. doi: 10.1161/HYPERTENSIONAHA.113.01516. Epub 2013 Aug 12.
3
Endothelin, kidney disease, and hypertension.内皮素、肾脏疾病与高血压。
Hypertension. 2013 Jun;61(6):1142-5. doi: 10.1161/HYPERTENSIONAHA.113.00595. Epub 2013 Apr 22.
4
Estrogen normalizes perinatal nicotine-induced hypertensive responses in adult female rat offspring.雌激素可使成年雌性幼鼠后代的围产期尼古丁诱导的高血压反应正常化。
Hypertension. 2013 Jun;61(6):1246-54. doi: 10.1161/HYPERTENSIONAHA.113.01152. Epub 2013 Mar 25.
5
Angiotensin II-mediated vascular changes in aged offspring rats exposed to perinatal nicotine.血管紧张素 II 介导的围生期尼古丁暴露的老年子代大鼠血管变化。
Peptides. 2013 Jun;44:111-9. doi: 10.1016/j.peptides.2013.02.019. Epub 2013 Mar 14.
6
Renal denervation abolishes the age-dependent increase in blood pressure in female intrauterine growth-restricted rats at 12 months of age.肾脏去神经支配可消除 12 月龄宫内发育受限雌性大鼠血压随年龄增长的增加。
Hypertension. 2013 Apr;61(4):828-34. doi: 10.1161/HYPERTENSIONAHA.111.00645. Epub 2013 Feb 19.
7
Role of leptin and central nervous system melanocortins in obesity hypertension.瘦素和中枢神经系统黑皮质素在肥胖性高血压中的作用。
Curr Opin Nephrol Hypertens. 2013 Mar;22(2):135-40. doi: 10.1097/MNH.0b013e32835d0c05.
8
Early life stress induces renal dysfunction in adult male rats but not female rats.早期生活应激会导致成年雄性大鼠的肾功能障碍,但不会导致成年雌性大鼠的肾功能障碍。
Am J Physiol Regul Integr Comp Physiol. 2013 Jan 15;304(2):R121-9. doi: 10.1152/ajpregu.00364.2012. Epub 2012 Nov 21.
9
Early-life sex-dependent vulnerability to oxidative stress: the natural twining model.生命早期性别依赖性氧化应激易感性:天然孪生模型
J Matern Fetal Neonatal Med. 2013 Feb;26(3):259-62. doi: 10.3109/14767058.2012.733751. Epub 2012 Oct 19.
10
Sex-specific programming of hypertension in offspring of late-gestation diabetic rats.糖尿病孕晚期大鼠对子代高血压的性别特异性编程。
Pediatr Res. 2012 Oct;72(4):352-61. doi: 10.1038/pr.2012.93. Epub 2012 Jul 17.

高血压发育编程中的性别差异。

Sex differences in the developmental programming of hypertension.

作者信息

Ojeda N B, Intapad S, Alexander B T

机构信息

Department of Pediatrics, University of Mississippi Medical Center, Jackson, MS, USA; Women's Health Research Center, University of Mississippi Medical Center, Jackson, MS, USA.

出版信息

Acta Physiol (Oxf). 2014 Feb;210(2):307-16. doi: 10.1111/apha.12206. Epub 2013 Dec 12.

DOI:10.1111/apha.12206
PMID:24268043
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4032374/
Abstract

Experimental models of developmental programming provide proof of concept and support Barker's original findings that link birthweight and blood pressure. Many experimental models of developmental insult demonstrate a sex difference with male offspring exhibiting a higher blood pressure in young adulthood relative to their age-matched female counterparts. It is well recognized that men exhibit a higher blood pressure relative to age-matched women prior to menopause. Yet, whether this sex difference is noted in individuals born with low birthweight is not clear. Sex differences in the developmental programming of blood pressure may originate from innate sex-specific differences in expression of the renin angiotensin system that occur in response to adverse influences during early life. Sex differences in the developmental programming of blood pressure may also involve the influence of the hormonal milieu on regulatory systems key to the long-term control of blood pressure such as the renin angiotensin system in adulthood. In addition, the sex difference in blood pressure in offspring exposed to a developmental insult may involve innate sex differences in oxidative status or the endothelin system or may be influenced by age-dependent changes in the developmental programming of cardiovascular risk factors such as adiposity. Therefore, this review will highlight findings from different experimental models to provide the current state of knowledge related to the mechanisms that contribute to the aetiology of sex differences in the developmental programming of blood pressure and hypertension.

摘要

发育编程的实验模型为概念验证提供了依据,并支持了巴克最初将出生体重与血压联系起来的研究结果。许多发育性损伤的实验模型都显示出性别差异,成年早期的雄性后代相对于年龄匹配的雌性后代血压更高。众所周知,在绝经前,男性相对于年龄匹配的女性血压更高。然而,出生体重低的个体是否存在这种性别差异尚不清楚。血压发育编程中的性别差异可能源于肾素血管紧张素系统表达中固有的性别特异性差异,这种差异是在生命早期受到不利影响时出现的。血压发育编程中的性别差异也可能涉及激素环境对血压长期控制关键调节系统的影响,如成年期的肾素血管紧张素系统。此外,暴露于发育性损伤的后代血压的性别差异可能涉及氧化状态或内皮素系统的固有性别差异,或者可能受到心血管危险因素(如肥胖)发育编程中年龄依赖性变化的影响。因此,本综述将重点介绍不同实验模型的研究结果,以提供与血压和高血压发育编程中性别差异病因机制相关的当前知识状态。