Uterine and nonuterine vascular responses to angiotensin II in ovine pregnancy

• Published in: The American journal of physiology Vol. 257; no. 1; p. H17
• Main Authors: Rosenfeld, C.R. (The University of Texas Southwestern Medical Center, Dallas, TX), Naden, R.P
• Format: Journal Article
• Language: English
• Published: United States 01.07.1989
• Subjects: ADIPOSE TISSUES; ADRENAL GLANDS; Angiotensin II - pharmacology; Animals; BLOOD CIRCULATION; Blood Pressure - drug effects; Cardiac Output - drug effects; CIRCULACION SANGUINEA; CIRCULATION SANGUINE; COEUR; CORAZON; Female; GESTACION; GESTATION; GLANDULAS SUPRARRENALES; HEART; Heart Rate - drug effects; OVIN; OVINOS; PEPTIDE; PEPTIDES; PEPTIDOS; Placenta - blood supply; PREGNANCY; Pregnancy, Animal - physiology; Regional Blood Flow - drug effects; SHEEP; SURRENALE; TEJIDO ADIPOSO; TISSU ADIPEUX; UTERO; UTERUS; Uterus - blood supply; Uterus - drug effects
• ISSN: 0002-9513; 2163-5773
• DOI: 10.1152/ajpheart.1989.257.1.H17

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 micrograms/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 less than 0.05); systemic responses exceeded uterine (P less than 0.05), except with 11.5 micrograms/min, when % delta UVR = % delta SVR, % delta UVR greater than % delta MAP, and UBF fell 29%. Although a dose-dependent rise in placental resistance occurred, blood flow was unaffected except at 11.5 micrograms ANG II/min, falling 16.8 +/- 3.5% (P = 0.059). In contrast, endometrial perfusion decreased 68 +/- 4.2 and 81 +/- 1.8% (P less than 0.01) with 5.73 and 11.5 micrograms ANG II/min, respectively. Myometrial responses were intermediate, thus placental flow increased from 75 to greater than 90% of total UBF. Adipose, renal, and adrenal glands were extremely sensitive to ANG II, with blood flows decreasing maximally at 0.573 micrograms/min (P less than 0.05). Maximum adipose vascular resistance occurred at 0.573 micrograms/min, greater than 400% (P less than 0.001), exceeding responses in all tissues (P less than 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.