In the current study, we investigated the expression and activity of ACE2 during pregnancy in normotensive and hypertensive rats, focusing on the relative contribution of the uterus and the placenta, the kidney serving as organ of eference. We used the Sabra rat model of salt-sensitive hypertension. We confirmed a systemic vasodilatory state during the third trimester of pregnancy, as evidenced by a reduction in blood pressure, both in normotensive and hypertensive rats. At the time that BP was reduced, ACE2 was expressed abundantly in the reproductive organs. The relative levels of ACE2 mRNA in the pregnant animal were placenta>kidneysuterus and of ACE2 activity kidney>placenta>uterus. In the uterus and the placenta, ACE2 expression was unaffected by strain, salt-loading or the level of blood pressure. ACE2 activity in the uterus of the non-pregnant rat was not affected by any of these variables either, but during pregnancy increased in salt-loaded animals. When estimating the total contribution of the uterus to ACE2 mRNA and activity, we found that during pregnancy, the amount of ACE2mRNA increased in both strains irrespective of diet, but that ACE2 activity increased in salt-loaded animals. We further estimated the relative total contribution of the uterus, placentas and kidneys to ACE2 expression and activity during pregnancy and found that the placentas were the major contributors, followed by the kidney and the uterus. We conclude that during pregnancy, the placentas in particular, but also the uterus, constitute important sources of ACE2, in addition to its normal production in the kidney, leading to an estimated two fold increase in total ACE2 activity. These data are consistent the hypothesis that transient ACE2 over-expression and increased activity during pregnancy may be important in modulating systemic as well as local hemodynamics in the utero-placental unit.