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1 Department of Pediatrics and 2 Department of Surgery and the Cardiovascular Center, University of Iowa, Iowa City, Iowa 52242
We previously demonstrated in fetal sheep that blockade of ANG
II type 1 (AT1) receptors did not attenuate an increase in right ventricle (RV) mass resulting from partial occlusion of the
pulmonary artery (PA). We have now determined the effects of
AT2-receptor blockade (PD-123319, 10 mg · kg
1 · day1 continuous
iv) on the response of the fetal RV to PA banding for 7 days. Four
groups of fetuses (each n = 7) were studied beginning at 126 ± 1 days gestation (term 145 days). RV weight-to-body
weight ratio (RV wt/body wt) increased (P < 0.05) in
PA-banded (6.00 ± 0.09 g/kg) and PA-banded + PD-123319
(6.19 ± 0.27 g/kg) compared with control (5.17 ± 0.17 g/kg)
and PD-123319-infused (5.27 ± 0.35 g/kg) fetuses (means ± SE). Blood pressure and heart rate were similar in all groups.
PD-123319 produced a decrease (P < 0.05) in
AT1 but not AT2 mRNA levels in both fetal
ventricles. To examine the effect of ANG II on fetal heart growth, twin
fetal sheep were infused with either ANG II (twin received vehicle) or
phenylephrine (Phe) (twin received vehicle) continuously for 7 days.
Mean arterial blood pressure was 20-25 mmHg higher in ANG II and
Phe fetuses compared with controls. The rate-pressure product was
similar in ANG II and Phe fetuses and 40-50% greater than
controls. Phe resulted in no change in RV wt/body wt or left ventricle-to-body weight ratio (LV wt/body wt) compared with controls. In contrast, ANG II produced a selective increase (27 ± 5%,
P < 0.05) in LV wt/body wt; no effect was seen on the
RV. ANG II produced a decrease (P < 0.05) in LV but
not RV AT1 mRNA levels compared with controls; no effect
was seen with Phe. The data demonstrate that in the ovine fetus,
AT2 receptors do not contribute to the maintenance of blood
pressure or the development of pressure-overload RV hypertrophy.
Elevated ANG II levels produce a selective increase in LV mass in the
fetal sheep that is, in part, independent of increased systolic load.
heart; phenylephrine; myocardium; development
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