The cardiovascular system undergoes profound changes during pregnancy. Maternal intravascular volume begins to increase in the first trimester rising an average of 45% by term.1 Cardiac output increases similarly2 and is redistributed to organs whose functions are crucial for a successful pregnancy. In the guinea pig, uterine artery (UA) blood flow increases 3500%, while mesenteric and renal artery blood flows increase only 90% and 10% respectively.3 Blood flow to the trunk actually diminishes. The mechanism underlying this redistribution is unknown. Coupled with the rise in cardiac output is a decrease in the systemic pressor response to angiotensin II (AII), norepinephrine(NE), and epinephrine.4–8 There is also a decrease in the contraction response among some but not all vascular beds. For example, contraction of UA to NE and thromboxane is characteristically reduced by pregnancy, whereas the response of the carotid artery is unaltered8–10 Since pregnancy does not alter neuroeffector mechanisms of NE such as release, receptor sensitivity, and accumulation11, changes in sympathetic control during pregnancy must be dependent on alterations at sites other than the neuroeffector junction. We have hypothesized that the mechanisms which alter vascular reactivity during pregnancy also mediate the redistribution of maternal cardiac output.9 We have further hypothesized that many of these mechanisms involve endothelium-dependent factors which are modulated by sex hormones.