Studies in anesthetized animals suggest that angiotensin II evokes a d
epressor as well as a presser effect, which becomes evident on cessati
on of infusion. We have studied 18 nonpregnant and 8, 23, and 22 women
in the first, second, and third trimesters of pregnancy to determine
whether such an effect is present in conscious women, whether it is do
se dependent, and whether it is influenced by pregnancy. Angiotensin I
I was infused intravenously in doubling concentrations at 10-minute in
tervals until a presser effect of approximate to 20 mm Hg was observed
. The infusion was stopped, and blood pressure was monitored at 2-minu
te intervals for 30 minutes. There was a significant diastolic depress
or effect after stopping angiotensin II in the nonpregnant women and t
hose in the second and third trimesters of pregnancy. Individual women
required differing doses of angiotensin II to evoke the standardized
presser response. It was thus possible to examine the depressor respon
se in each group in relation to infused doses of angiotensin II. In no
npregnant women and in those in the second and third trimesters of pre
gnancy, the depressor response was dose dependent (P<.001). At any giv
en dose, the depressor response deepened as pregnancy progressed (P<.0
01). Basal plasma prostacyclin concentrations rise in pregnancy, and a
ngiotensin II can stimulate prostacyclin synthesis. This might mediate
the depressor effect. In conclusion, the diminished presser response
to angiotensin II in normal pregnancy may be partly due to an increasi
ng depressor effect of the hormone.