(Hypertension. 1995;25:626-630.)
© 1995 American Heart Association, Inc.
Articles |
11ß-Hydroxysteroid Dehydrogenase and Its Inhibitors in Hypertensive Pregnancy
From the Department of Medicine, University of Edinburgh, Western General Hospital, Edinburgh, Scotland, UK (B.R.W., C.R.W.E.); the Department of Medicine, University of New South Wales, St George Hospital, Kogarah, NSW, Australia (P.M.W., M.A.B., J.A.W.); and the Department of Chemical Pathology, University College London Hospitals, London, UK (J.W.H.).
Abstract Preeclampsia is accompanied by amplification of the sodium retention that is a feature of normal pregnancy. Recent evidence suggests that mineralocorticoid receptor activation is increased in preeclampsia, but classic mineralocorticoids (aldosterone, 11-deoxycorticosterone) are not present in excess. Cortisol can act as a mineralocorticoid receptor agonist only when its renal inactivation to cortisone by 11ß-hydroxysteroid dehydrogenase is impaired, for example, in congenital enzyme deficiency and after administration of exogenous inhibitors (eg, licorice). Endogenous inhibitors of this enzyme have been detected in human urine and are increased in pregnancy. To establish whether cortisol causes mineralocorticoid excess in hypertensive pregnancy and whether endogenous inhibitors of 11ß-hydroxysteroid dehydrogenase are responsible, we studied 25 hypertensive pregnant patients (13 with preeclampsia and 12 with gestational hypertension), 16 normotensive pregnant subjects, and 13 nonpregnant control subjects. Concentrations of plasma renin and aldosterone were increased in pregnancy, but less so in hypertensive pregnancy. Plasma potassium and urinary electrolytes were not different between the groups. Plasma cortisol was increased in pregnancy but not different in hypertensive pregnancy, and urinary cortisol, plasma and urinary cortisone, and urinary tetrahydrocortisol and tetrahydrocortisone were not different between the groups. Endogenous inhibitors of 11ß-hydroxysteroid dehydrogenase were more active in urine from pregnant women but were not increased further in hypertensive pregnancy. There were no differences in these parameters between patients with preeclampsia and gestational hypertension. We conclude that deficient inactivation of cortisol to cortisone does not contribute to the sodium retention of normotensive or hypertensive pregnancy and that endogenous inhibitors of 11ß-hydroxysteroid dehydrogenase have no evident pathophysiological significance in pregnancy.
Key Words: hydroxysteroid dehydrogenases • adrenal cortex hormones • blood pressure • hypertension, pregnancy-induced • pregnancy • preeclampsia • adrenal glands
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