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Department of Pediatrics, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75235
The uterine vasculature of women and sheep predominantly expresses type
2 ANG II receptors that do not mediate vasoconstriction. Although
systemic ANG II infusions increase uterine vascular resistance (UVR),
this could reflect indirect mechanisms. Thus we compared systemic and
local intra-arterial ANG II infusions in six near-term pregnant and
five ovariectomized nonpregnant ewes to determine how ANG II increases
UVR. Systemic ANG II dose-dependently (P > 0.001) increased
arterial pressure (MAP) and UVR and decreased uterine blood flow (UBF)
in pregnant and nonpregnant ewes; however, nonpregnant responses
exceeded pregnant (P < 0.001). In contrast, local ANG II
infusions at rates designed to acheive concentrations in the uterine
circulation comparable to those seen during systemic infusions did not
significantly decrease UBF in either group, and changes in MAP and UVR
were absent or markedly attenuated. When MAP rose during local ANG II,
which only occurred with doses 
2 ng/ml, increases in MAP were delayed
more than twofold compared with responses during systemic ANG II
infusions and always preceded decreases in UBF, resembling that
observed during systemic ANG II infusions. These observations
demonstrate attenuated uterine vascular responses to systemic ANG II
during pregnancy and suggest that systemic ANG II may increase UVR
through release of another potent vasoconstrictor(s) into the systemic circulation.
angiotensin receptors; nonpregnant; pregnancy; uteroplacental circulation; uterine blood flow
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