It has been suggested previously that norepinephrine does not change fetal placental vascular resistance but does change placental blood flow by changing fetal heart rate. We have tested the hypothesis that fetal heart rate is a determinant of fetal placental blood flow by observing changes in placental vascular resistance in 10 chronically catheterized near-term sheep fetuses. Pressures and flow were observed in the control condition and 150 s after the initiation of infusion of norepinephrine at 50 micrograms/min. The fetuses were then given 1.5 mg of atropine and control observations were again made. The norepinephrine infusion was repeated and pressures and blood flows were measured after 150 s. Atropine increased the fetal heart rate from 168 +/- 6 to 205 +/- 12 beats/min. Placental vascular resistance did not change. Norepinephrine resulted in bradycardia, hypertension and an increased placental vascular resistance. After pretreatment with atropine, norepinephrine resulted in tachycardia, hypertension and an increased placental vascular resistance. We conclude that fetal heart rate is not a major determinant of blood flow and that high doses of norepinephrine cause vasoconstriction of the placental vascular bed of the near-term sheep fetus.