Abstract Title

Uterine perivascular adipose tissue potentiates vasoconstriction in maternal arteries during rat pregnancy

RAD Assignment Number

422

Presenter Name

Oluwatobiloba Osikoya

Abstract

Background: Perivascular adipose tissue (PVAT) functions mostly to increase vasodilation in healthy conditions, but increases vasoconstriction in diseased states. During pregnancy, adipose tissue expands, and uterine arteries (UTA) undergo substantial remodeling. Previously, our laboratory showed that uterine PVAT potentiates contractile responses in UTA from pregnant but not in arteries from non-pregnant rats. It is unknown, however, if the effects of uterine PVAT are vascular bed specific and if they are mediated by pregnancy.

Hypothesis: Uterine PVAT potentiates contractions in maternal arteries independently of vascular bed and this pro-contractile property is mediated by pregnancy specific factors.

Methods: Sprague-Dawley pregnant rats were sacrificed on gestational day 16 (term=21-22) and aged-matched non-pregnant rats were used as controls. Uterine PVAT, and isolated segments of UTA and mesenteric arteries (MES) mounted onto a wire myograph. To determine whether uterine PVAT has pro-contractile effects independently of vascular bed, pregnant UTA and MES were incubated with uterine PVAT (0.1 g) for 30 minutes. To determine whether the pro-contractile effects of uterine PVAT are mediated by pregnancy specific changes, UTA from pregnant and non-pregnant rats were incubated for 30 minutes with non-pregnant PVAT (0.1 g) and pregnant PVAT (0.1 g), respectively. Concentration response curves to potassium chloride (KCl, 4.7 – 80 mM) were performed in all arteries. Force generated at each KCl concentration was expressed in mN and area under the curve (AUC) was used to quantify total contraction.

Results: MES from pregnant rats had increased contractile responses to KCl when incubated with uterine PVAT (AUC, -PVAT: 366±46 vs. +PVAT: 529±53, P = 0.02). UTA from pregnant rats had increased contractile responses to KCl when incubated with uterine PVAT (AUC, -PVAT: 893±40 vs. +PVAT: 1092±59, p=0.004). Preliminary data showed that PVAT from non-pregnant rats increased contractile responses in UTA from pregnant rats (KCl 30 mM, -PVAT: 4.7±0.9 mN vs. +PVAT: 11.4±1.4 mN, p=0.047). Pregnant PVAT had no effect on UTA from non-pregnant rats (p>0.05).

Conclusions: Uterine perivascular adipose tissue potentiates vasoconstriction in both uterine and mesenteric arteries from pregnant rats. These effects may be due to vascular remodeling during pregnancy.

Research Area

Cardiovascular

Presentation Type

Poster

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Uterine perivascular adipose tissue potentiates vasoconstriction in maternal arteries during rat pregnancy

Background: Perivascular adipose tissue (PVAT) functions mostly to increase vasodilation in healthy conditions, but increases vasoconstriction in diseased states. During pregnancy, adipose tissue expands, and uterine arteries (UTA) undergo substantial remodeling. Previously, our laboratory showed that uterine PVAT potentiates contractile responses in UTA from pregnant but not in arteries from non-pregnant rats. It is unknown, however, if the effects of uterine PVAT are vascular bed specific and if they are mediated by pregnancy.

Hypothesis: Uterine PVAT potentiates contractions in maternal arteries independently of vascular bed and this pro-contractile property is mediated by pregnancy specific factors.

Methods: Sprague-Dawley pregnant rats were sacrificed on gestational day 16 (term=21-22) and aged-matched non-pregnant rats were used as controls. Uterine PVAT, and isolated segments of UTA and mesenteric arteries (MES) mounted onto a wire myograph. To determine whether uterine PVAT has pro-contractile effects independently of vascular bed, pregnant UTA and MES were incubated with uterine PVAT (0.1 g) for 30 minutes. To determine whether the pro-contractile effects of uterine PVAT are mediated by pregnancy specific changes, UTA from pregnant and non-pregnant rats were incubated for 30 minutes with non-pregnant PVAT (0.1 g) and pregnant PVAT (0.1 g), respectively. Concentration response curves to potassium chloride (KCl, 4.7 – 80 mM) were performed in all arteries. Force generated at each KCl concentration was expressed in mN and area under the curve (AUC) was used to quantify total contraction.

Results: MES from pregnant rats had increased contractile responses to KCl when incubated with uterine PVAT (AUC, -PVAT: 366±46 vs. +PVAT: 529±53, P = 0.02). UTA from pregnant rats had increased contractile responses to KCl when incubated with uterine PVAT (AUC, -PVAT: 893±40 vs. +PVAT: 1092±59, p=0.004). Preliminary data showed that PVAT from non-pregnant rats increased contractile responses in UTA from pregnant rats (KCl 30 mM, -PVAT: 4.7±0.9 mN vs. +PVAT: 11.4±1.4 mN, p=0.047). Pregnant PVAT had no effect on UTA from non-pregnant rats (p>0.05).

Conclusions: Uterine perivascular adipose tissue potentiates vasoconstriction in both uterine and mesenteric arteries from pregnant rats. These effects may be due to vascular remodeling during pregnancy.