|
pubmed:abstractText |
Animal data show that decreased activity of placental 11-beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2), which potently inactivates glucocorticoids (e.g. cortisol) to inert forms (cortisone), allows increased access of maternal glucocorticoids to the fetus and 'programs' hypertension. Data in humans are limited. We examined in humans the association between venous umbilical cord blood glucocorticoids, a potential marker for placental 11beta-HSD2 enzyme activity, and blood pressure at age 3 years.
|
