Pregnancy

Reduced Utero-Placental Perfusion Alters Uterine Arcuate Artery Function in the Pregnant Sprague-Dawley Rat

Abstract
Evidence continues to implicate reduced placental perfusion as the cause of preeclampsia, initiating a sequence of events leading to altered vascular function and hypertension. This study was designed to determine the influence of reduced utero-placental perfusion pressure on responsiveness of uterine arcuate resistance arteries. Reduced utero-placental perfusion pressure (RUPP) was surgically induced in pregnant Sprague-Dawley rats on gestational day 14. On gestational day 20, uterine arcuate arteries were mounted on a small vessel wire myograph and challenged with incremental concentrations of vasoconstrictors and vasorelaxants for measurement of isometric tension. Uterine arteries from the RUPP group demonstrated an increased maximal tension in response to phenylephrine (p < 0.01), potassium chloride at 30mM (p < 0.05), 60 mM (p < 0.01) and 120 mM (p < 0.01) and angiotensin II (p < 0.05), as compared to the sham-operated controls. In arteries from RUPP and sham-operated control groups, endothelium-dependent relaxation in response to acetylcholine (p < 0.05)and calcium ionophore (A23187) (p < 0.05) was significantly reduced in the RUPP group. Fetal growth indices including litter size, fetal and placental weight were significantly smaller in the RUPP group than in the fetus' of sham-operated controls, consistent with significant growth restriction. Data suggest that reduced utero-placental perfusion promotes hyperresponsiveness and impaired endothelium-dependent relaxation in uterine arcuate arteries, leading to intrauterine fetal growth restriction.

Key words: Pregnancy • Nitric oxide • Placenta • Uterus

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