The uteroplacental vasculature is more refractory to angiotensin II (ANG II) than the systemic vasculature as a whole. To ascertain the differences in responses between reproductive and nonreproductive tissues that account for this, we infused ANG II (0.573, 5.73, and 11.5 μg/min) in pregnant sheep (137 ± 5 days of gestation) and monitored arterial pressure (MAP), heart rate, and uterine blood flow (UBF); cardiac output and regional blood flows were measured with radiolabeled microspheres. Dose-dependent changes in MAP, UBF, and systemic (SVR) and uterine (UVR) vascular resistance occurred (P < 0.05); systemic responses exceeded uterine (P < 0.05), except with 11.5 μg/min, when %ΔUVR = %ΔSVR, %ΔUVR > %ΔMAP, and UBF fell 29%. Although a dose-dependent rise in placental resistance occurred, blood flow was unaffected except at 11.5 μg ANG II/min, falling 16.8 ± 3.5% (P = 0.059). In contrast, endometrial perfusion decreased 68 ± 4.2 and 81 ± 1.8% (P < 0.01) with 5.73 and 11.5 μg ANG II/min, respectively. Myometrial responses were intermediate, thus placental flow increased from 75 to > 90% of total UBF. Adipose, renal, and adrenal glands were extremely sensitive to ANG II, with blood flows decreasing maximally at 0.573 μg/min (P < 0.05). Maximum adipose vascular resistance occurred at 0.573 μg/min, > 400% (P < 0.001), exceeding responses in all tissues (P < 0.05). The placenta is less responsive to ANG II than other uterine and most nonreproductive tissues, resulting in preferential maintenance of uteroplacental perfusion and protecting the fetus from the effects of this vasoconstrictor.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|State||Published - Jan 1 1989|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)