1. The effect of doubling doses of angiotensin II on maternal systemic blood pressure and arcuate and fetal umbilical artery Doppler velocity profiles has been investigated in 10 women in first- and 10 in second-trimester pregnancy. Ten non-pregnant women were also studied.

2. A progressive decrease in the pressor response to angiotensin II in early pregnancy as previously described was confirmed.

3. Angiotensin II induced a significant dose-dependent increase in the pulsatility index (a measure of downstream resistance) in the umbilical artery in both first- and second-trimester patients. There was an apparent increase in the threshold response of the pulsatility index to angiotensin II in the umbilical artery as pregnancy progressed. There was also a significant correlation between changes in maternal systolic or diastolic pressure and change in umbilical artery pulsatility index, but this did not differ between the two trimesters. This suggests that the increase in pulsatility index is related to blood pressure rather than angiotensin II. This is consistent with reports that angiotensin II does not cross the haemo-monochorial placenta.

4. Basal pulsatility index in the arcuate artery fell with increasing gestation. There was a significant inverse association between the evoked change in maternal systemic blood pressure and the change in arcuate artery pulsatility index, suggesting local vasodilatation.

5. We conclude that acutely increasing maternal blood pressure leads to increased vascular resistance on the fetal side of the circulation.

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