GLUCOCORTICOID EXPOSURE INUTERO - NEW MODEL FOR ADULT HYPERTENSION

被引：715

作者：

BENEDIKTSSON, R ^{[1
]}

LINDSAY, RS ^{[1
]}

NOBLE, J ^{[1
]}

SECKL, JR ^{[1
]}

EDWARDS, CRW ^{[1
]}

机构：

[1] UNIV EDINBURGH,WESTERN GEN HOSP,DEPT MED,EDINBURGH EH4 2XU,MIDLOTHIAN,SCOTLAND

来源：

LANCET | 1993年 / 341卷 / 8841期

基金：

英国惠康基金;

关键词：

D O I：

10.1016/0140-6736(93)90138-7

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Hypertension is strongly predicted by the combination of low birthweight and a large placenta. This association could be due to increased fetal exposure to maternal glucocorticoids. Fetal protection is normally effected by placental 11beta-hydroxysteroid dehydrogenase (11beta-OHSD), which converts physiological glucocorticoids to inactive products. We found that rat placental 11beta-OHSD activity correlated positively with term fetal weight and negatively with placental weight. Offspring of rats treated during pregnancy with dexamethasone (which is not metabolised by 11beta-OHSD) had lower birthweights and higher blood pressure when adult than did offspring of control rats. Increased fetal glucocorticoid exposure secondary to attenuated placental 11beta-OHSD activity may link low birthweight and high placental weight with hypertension.

引用

页码：339 / 341

页数：3

共 10 条

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