Asymmetrisches Dimethylarginin (ADMA): Ein endogener Hemmstoff der NO-Synthase - und auch ein Risikomarker der Präeklampsie?

Abstract

Preeclampsia still is one of the major causes of maternal and neonatal morbidity and death. The causes of preeclampsia are multifactorial, but a common pathway of vascular impairment in preeclampsia is endothelial dysfunction. The endothelium plays a crucial role in regulating physiological vascular tone and structure as well as in the vascular adaptations to pregnancy. The major mediator responsible for this is nitric oxide (NO). NO formation is inhibited by asymmetric dimethylarginine (ADMA), an endogenous analogue of L-arginine. ADMA plasma levels are increased in patients at high cardiovascular risk. Several clinical studies have produced evidence to show that preeclampsia is associated with elevated ADMA plasma concentrations as compared to healthy pregnant women. In animal models, preeclampsia can be incuced by administration of NO synthase inhibitors. Therefore, ADMA may be a novel marker of the risk of preeclampsia, like it is a marker of cardiovascular risk in general. Administration of L-arginine can antagonize the adverse effects of ADMA on the vasculature; L-arginine has also been shown to reduce elevated blood pressure in pregnant women.