Benediktsson R, Lindsay R S, Noble J, Seckl J R, Edwards C R
University of Edinburgh, Department of Medicine, Western General Hospital, UK.
Lancet. 1993 Feb 6;341(8841):339-41. doi: 10.1016/0140-6736(93)90138-7.
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 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD), which converts physiological glucocorticoids to inactive products. We found that rat placental 11 beta-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 11 beta-OHSD) had lower birthweights and higher blood pressure when adult than did offspring of control rats. Increased fetal glucocorticoid exposure secondary to attenuated placental 11 beta-OHSD activity may link low birthweight and high placental weight with hypertension.
低出生体重和胎盘过大共同作用,强烈预示着高血压。这种关联可能是由于胎儿接触母体糖皮质激素增加所致。胎儿的保护通常由胎盘11β-羟基类固醇脱氢酶(11β-OHSD)实现,该酶可将生理性糖皮质激素转化为无活性产物。我们发现,大鼠胎盘11β-OHSD活性与足月胎儿体重呈正相关,与胎盘重量呈负相关。孕期用不被11β-OHSD代谢的地塞米松处理的大鼠所产后代,成年后出生体重较低且血压较高,而对照组大鼠后代则不然。胎盘11β-OHSD活性减弱导致胎儿糖皮质激素暴露增加,可能将低出生体重和高胎盘重量与高血压联系起来。