Glucocorticoid exposure in utero: new model for adult hypertension
- PMID: 8094115
- DOI: 10.1016/0140-6736(93)90138-7
Glucocorticoid exposure in utero: new model for adult hypertension
Erratum in
- Lancet 1993 Feb 27;341(8844):572
Abstract
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.
Comment in
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Parity, birthweight, and cortisol.Lancet. 1993 Mar 27;341(8848):828. doi: 10.1016/0140-6736(93)90602-d. Lancet. 1993. PMID: 8096027 No abstract available.
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Low-birthweight hypertension via enzyme and receptor imprintings of glucocorticoid.Lancet. 1993 Jul 31;342(8866):303-4. doi: 10.1016/0140-6736(93)91849-h. Lancet. 1993. PMID: 8101326 No abstract available.
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