Abstract.We conducted a prospective and serial study of blood pressure (BP) and of the changes in the renin‐angiotension‐aldosterone system (RAAS) and of one factor in the kallikrein‐kinin system during normal pregnancy and in patients with pre‐existing or developing hypertension in pregnancy. Strict diagnostic criteria were used to define pre‐eclampsia (PE), essential hypertensives (EH) and other hypertension (OH) in pregnancy.In normotensive pregnant women (n = 26) there was a rise in all components of the RAAS measured: plasma renin activty (PRA), plasma aldosterone concentration (PAC) and urinary aldosterone excretion (tU‐Aldo), from week 12 to week 20 of pregnancy, compared with non‐pregnant control subjects (n = 24) of similar age. Peak values were observed at week 30, whereafter fairly constant levels were maintained. Plasma and urinary aldosterone levels were increased 6‐10 fold. Urinary kallikrein excretion (tU‐Kall) was increased at weeks 12‐20, but at weeks 30‐36 roughly the same mean values were observed as for non‐pregnant control subjects.On the other hand, different results were obtained in the hypertensive patients, especially those with PE (n = 18). PRA was depressed in the PE group to values about those observed in non‐pregnant control subjects. PRA was also significantly lower in the PE group than in EH (n = 8) or OH (n=16) groups. PAC and tU‐Ado were also much lower in PE patients than in normal pregnant women at comparable gestational ages, but not significantly different from EH patients, whereas those with OH had both PAC and tU‐Pldo values comparable to normal pregnant women.In the PE group, tU‐Kall was significantly lower than for all other groups, but tU‐Kall values for EH and OH groups did not differ from those of normal pregnant women at the same gestational age.We conclude that during normal pregnancy there is an early and very marked activation of the RAAS. Initially, the kallikrein‐kinin system also seems to be activated. With the development of or with pre‐existing hypertension, the activation of RAAS is diminished. The suppression of both renin and aldosterone is most obvious in PE. Concomitantly, tU‐Kall decreases in PE patients, which may contribute to the rise in BP due to