THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM IN PREECLAMPSIA

Pre-eclampsia is characterised physiologically by plasma volume contra ction, intravascular coagulation and intense vasoconstriction. It was originally thought that the renin-angiotensin-aldosterone (RAA) system would be overactive but studies have shown a more complex picture. Pl asma renin activity (PRA) and concentration (PRC) and plasma angiotens in II (AII) and aldosterone concentrations (PAC) are reduced compared to normal pregnancy. Total renin concentration is normal and plasma co ncentrations of high molecular weight angiotensinogen are increased in pre-eclampsia though total angiotensinogen is normal. PRA and PRC res pond appropriately to physiologic stimuli in pre-eclampsia except for impaired renin release following frusemide, possibly due to prostacycl in deficiency. Although plasma AII concentrations are reduced there is heightened presser sensitivity to infused AII - the mechanism(s) for this are unknown. PAC is reduced but the ratio PAC:PRC is twofold grea ter in pre-eclampsia than normal pregnancy. This does not appear to be due to changes in potassium, atrial natriuretic peptide, dopamine or ACTH, and may be another manifestation of increased (adrenal) sensitiv ity to AII in pre-eclampsia. There is an inverse relationship between the plasma active renin to prorenin ratio and the clinical severity of pre-eclampsia. Understanding the mechanisms producing these changes i n the RAA system in pre-eclampsia will give strong clues to the overal l pathogenesis of this disorder.