11β-hydroxysteroid dehydrogenase (11β-HSD-II) activity in human placenta: Its relationship to placental weight and birth weight and its possible role in hypertension

Abstract

It has been assumed that low birth weight and high placenta weight were key factors for predicting hypertension in human adulthood. Adeficiency in placental 11β-HSD-II enzyme activity was supposed to be the underlying cause. To possibly establish 11β-HSD-II as a leading factor, we determined 11β-HSD-II activities in 133 healthy pregnancies, 21 proteinuric pregnancies complicated by pregnancy-induced hypertension (PIH), 26 non proteinuric PIH pregnancies and 15 pregnancies complicated by fetal growth restriction (32^nd–41^st gestational week). We could not identify differences in 11β-HSD-II activity between pregnancies with the rare combination of small babies with big placentas and others (p 5 0,59; Kruskal-Wallis test). And although there was no correlation between 11β-HSD-II activity and birth weight, in the control gestational age correlated with 11β-HSD-II activity (r = 0,22; p < 0.05; Spearman).

11β-HSD-II activity in the proteinuric PIH group was significantly higher than in the controls (11,7 pmol/min/mg prot.; range 10–13,2 vs. 7,9; range 7,0–9,1; p < 0,05). The lowest, but not significant, enzyme activities were in the IUGR group (5,8 pmol/min/mg prot.; range 4,0–9,2). In this group, analysis of variance detected a correlation between enzyme activity and placental weight.

In conclusion, we could not confirm that placental 11β-HSD-II deficiencies act as an indicator for the risk of adult hypertension in small fetuses with large placentas. However, in growth restriction 11β-HSD-II activity might play a role. To clarify the influence in this group, further research is needed.

Increased 11β-HSD-II activities with gestational age in the control may serve to sustain fetal adrenal steroid genesis and to prepare the fetus for autonomic life.