The 24-hour urinary excretion of kallikrein (K), and prostaglandin E2 (PGE2), which reflects their intrarenal synthesis, was measured in 7 normal women (NW), 10 women with essential hypertension (EH), 26 normal pregnant women (NP), 12 women with hypertension in pregnancy (HP), and 4 women with toxemia. All pregnant women were in the last trimester of their pregnancy (week 24-40). K was raised in NP (99.6 ± 8.1 KU/24 h) and HP (106.5 ± 8 KU/24 h) compared to NW (57 ± 8.23 KU/24 h) (p < 0.05). PGE2 excretion was decreased in EH (403.25 ± 90.6 ng/24 h) compared to NW (508.6 ± 80.26 ng/24 h). During pregnancy PGE2 was increased to 1,088 ± 93.2 ng/24 h in NP and significantly more in HP, 1,885 ± 40 ng/24 h (p < 0.002). In this regard it differed from K. These data may suggest that, in addition to K, other factors (as angiotensin II and/or antidiuretic hormone) possibly activate renal PGE2 production in HP. In toxemia, K (23 ± 65.1 KU/24 h) and PGE2 (583 ± 172.83 ng/24 h) were markedly decreased. The above results suggest that the renal kallikrein-kinin and prostaglandin systems may play a role in sodium homeostasis during pregnancy. Their exact influence on the pathogenesis of hypertension in nonpregnant, pregnant, and toxemic subjects awaits further investigation.