C. R. W. Edwards

TL;DR: Findings seem to explain why sodium retention, hypokalaemia, and hypertension develop in subjects with congenital deficiency of 11 beta-OHSD and those in whom the enzyme has been inhibited by liquorice.

TL;DR: It was found that rat placental 11 beta-OHSD activity correlated positively with term fetal weight and negatively with placental weight, and offspring of rats treated during pregnancy with dexamethasone had lower birthweights and higher blood pressure when adult than did offspring of control rats.

TL;DR: It is suggested that in both conditions there is a defect in the renal conversion of cortisol to cortisone by 11 beta-OHSD which results in high intrarenal cortisol levels, acting on type 1 mineralocorticoid receptors to cause sodium retention.

TL;DR: The lifetime risk of common disorders may be partly determined by the intrauterine environment, supported by findings that in rats decreased activity of the enzyme that acts as a placental barrier to maternal glucocorticoids is associated with low birthweight.

TL;DR: The nutritional manipulation during pregnancy significantly increased systolic blood pressure in the resulting offspring in early adulthood, suggesting a possible common pathway whereby maternal environmental factors may influence fetal and placental growth and programme disease is inferred.