Control of vascular responsiveness during human pregnancy

Over 40 years ago, Dieckmann and Michel reported that vascular reactivity to the pressor effects of a vasoactive agent (crude vasopressin) is greater in preeclamptic than in normotensive pregnant women [1]. In 1956, Raab et al found similar responses to the infusion of catecholamines [2]. Neither of these groups of investigators found a significant difference in the pressor response between nonpregnant subjects and normal pregnant controls. In 1961, however, Abdul-Karim and Assali found that the pressor response to a standard dose of angiotensin II (AII) late in normal pregnancy was much less than that observed after delivery; that is, the pregnant women were relatively refractory to the pressor effects of infused AII [3]. In 1968, Talledo, Chesley, and Zuspan reported that preeclamptic women were as sensitive to AH as were nonpregnant subjects. The preeclamptic subjects appeared to have lost their pregnancy-associated refractoriness to AII [4]. These authors conjectured that the relative refractoriness to AII that occurred in normal pregnancy might be the consequence of an elevated plasma concentration of AII. Notably, a similar refractoriness to the pressor effects of injected AII is exhibited by patients with secondary aldosteronism and in patients with congestive heart failure or cirrhosis with ascites [5, 6].