Pre-eclampsia is characterised physiologically by plasma volume contraction, 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. Plasma renin activity (PRA) and concentration (PRC) and plasma angiotensin II (AII) and aldosterone concentrations (PAC) are reduced compared to normal pregnancy. Total renin concentration is normal and plasma concentrations of high molecular weight angiotensinogen are increased in pre-eclampsia though total angiotensinogen is normal. PRA and PRC respond appropriately to physiologic stimuli in pre-eclampsia except for impaired renin release following frusemide, possibly due to prostacyclin deficiency. Although plasma AII concentrations are reduced there is heightened pressor sensitivity to infused AII--the mechanism(s) for this are unknown. PAC is reduced but the ratio PAC-PRC is twofold greater 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) sensitivity to AII in pre-eclampsia. There is an inverse relationship between the plasma active renin to prorenin ratio and the clinical severity of the pre-eclampsia. Understanding the mechanisms producing these changes in the RAA system in pre-eclampsia will give strong clues to the overall pathogenesis of this disorder.