Uterine distension differentially affects remodelling and distensibility of the uterine vasculature in non-pregnant rats.

During pregnancy the mammalian uterine circulation undergoes significant expansive remodelling necessary for normal pregnancy outcome. The underlying mechanisms are poorly defined. The goal of this study was to test the hypothesis that myometrial stretch actively stimulates uterine vascular remodelling by developing a new surgical approach to induce unilateral uterine distension in non-pregnant rats.

Endothelial-derived hyperpolarization factor (EDHF) contributes to PlGF-induced dilation of mesenteric resistance arteries from pregnant rats.

The aim of this study was to investigate the cellular mechanism involved in the potent vasodilatory action of PlGF on mesenteric resistance arteries from pregnant rats. PlGF (3 nM) induced a vasodilation of 64 ± 3.8% that was completely abolished by endothelial denudation.

Effects of pregnancy, hypertension and nitric oxide inhibition on rat uterine artery myogenic reactivity.

Background/aims: The purpose of this study was to examine the effects of hypertension and nitric oxide (NO) inhibition on myogenic tone in uterine arteries during pregnancy.

Methods: Premyometrial radial uterine arteries from nonpregnant and late pregnant Sprague-Dawley rats were evaluated for myogenic reactivity from the following groups: control, hypertensive/NO-inhibited (L-NAME treatment) and normotensive/NO-inhibited (L-NAME plus hydralazine).

Results: In both nonpregnant and pregnant animals, L-NAME treatment significantly elevated blood pressures, while the addition of hydralazine made the animals normotensive.

Mechanisms underlying maternal venous adaptation in pregnancy.

To define the effects of pregnancy on mechanical properties and reactivity, mesenteric veins from late pregnant and virgin control (nonpregnant) rats were pressurized to determine gestational changes in size and distensibility. Reactivity studies used an adrenergic constrictor (norepinephrine) and an endothelium-mediated vasodilator (acetylcholine). The contribution of nitric oxide to endothelial function was evaluated with pharmacologic inhibition of nitric oxide synthase.

Inhibition of nitric oxide synthases abrogates pregnancy-induced uterine vascular expansive remodeling.

Background/aims: It was the aim of this study to test the hypothesis that hypertension and/or inhibition of nitric oxide (NO) synthases alters uterine vascular remodeling during pregnancy.

Methods: Using a model of hypertension (NO synthase inhibition with L-NAME) in nonpregnant and pregnant rats, comparisons were made with age-matched controls, as well as with animals receiving hydralazine along with L-NAME to maintain normotension in the presence of NO synthase inhibition. Circumferential and axial remodeling of large (main uterine, MUA) and small (premyometrial radial) arteries were quantified and compared.

Predominance of local over systemic factors in uterine arterial remodeling during pregnancy.

This study used a rat model in which pregnancy was surgically restricted to one uterine horn to differentiate between local (fetoplacental) and systemic (endocrine) influences on uterine vascular remodeling during pregnancy. Sprague-Dawley rats with single-horn pregnancies were studied on day 20/22 of gestation and compared to age-matched nonpregnant and late-pregnant controls. The morphology (axial length, lumen diameter, wall thickness) of the main uterine artery and of smaller arcuate vessels showed that vascular growth was dramatically increased in the pregnant versus nonpregnant horn, (P < .

Placental growth factor is a potent vasodilator of rat and human resistance arteries.

The objectives of this study were to determine whether placental growth factor (PlGF) exerts a vasodilatory effect on rat uterine vessels (arcuate arteries and veins) and to examine regional differences in reactivity by comparing these responses to those of comparably sized mesenteric vessels. We also sought to examine and compare its effects on human uterine and subcutaneous vessels. All vessels were studied in vitro, under pressurized (rat) or isometric wire-mounted (human) conditions, and exposed to a range of PlGF concentrations.