Increased myogenic reactivity of uterine arteries from pregnant rats with reduced uterine perfusion pressure

Reho, John J; Toot, Jonathan; Peck, Jennifer; Novak, Jacqueline; Yun, Yang; Ramirez, Rolando

doi:10.1016/j.preghy.2011.11.005

Cited by 17 publications

(14 citation statements)

References 32 publications

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“…Ex vivo, vessels from women with preeclampsia showed increased responsiveness to numerous constrictors, including KCl and arginine vasopressin [105]. Comparable findings have been shown in the rat RUPP model of preeclampsia; uterine and mesenteric vessels from RUPP dams show increased myogenic reactivity [110,113,114], and increased constriction in response to pressors [5,6]. However, others report no change in constrictor capacity [110,113,114].…”

Section: The Maternal Systemic Vasculature -Endothelial Dysfunctionmentioning

confidence: 77%

“…Comparable findings have been shown in the rat RUPP model of preeclampsia; uterine and mesenteric vessels from RUPP dams show increased myogenic reactivity , and increased constriction in response to pressors . However, others report no change in constrictor capacity . Recently, Abdalvand and colleagues found that mesenteric arteries from RUPP dams show enhanced contractility to bET‐1, resulting from altered conversion to ET‐1 within the endothelium .…”

Section: Placental Ischemiamentioning

confidence: 78%

“…Alterations in endothelium‐dependent relaxation have also been investigated in the rat RUPP model of preeclampsia. Deficits in endothelium‐dependent relaxation have been noted in uterine and mesenteric arteries; reports range from a significant reduction in relaxation to no change relative to normal‐pregnant animals . In the aorta, a substantial decrease in relaxation has been noted in some studies , while others report a more subtle change .…”

Section: Placental Ischemiamentioning

confidence: 99%

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Vascular Dysfunction in Preeclampsia

2014

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Preeclampsia is a complex disorder which affects an estimated 5% of all pregnancies worldwide. It is diagnosed by hypertension in the presence of proteinuria after the 20th week of pregnancy and is a prominent cause of maternal morbidity and mortality. As delivery is currently the only known treatment, preeclampsia is also a leading cause of preterm delivery. Preeclampsia is associated with maternal vascular dysfunction, leading to serious cardiovascular risk both during and following pregnancy. Endothelial dysfunction, resulting in increased peripheral resistance, is an integral part of the maternal syndrome. While the cause of preeclampsia remains unknown, placental ischemia resulting from aberrant placentation is a fundamental characteristic of the disorder. Poor placentation is believed to stimulate the release of a number of factors including pro- and antiangiogenic factors and inflammatory activators into the maternal systemic circulation. These factors are critical mediators of vascular function and impact the endothelium in distinctive ways, including enhanced endothelial oxidative stress. The mechanisms of action and the consequences on the maternal vasculature will be discussed in this review.

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Section: The Maternal Systemic Vasculature -Endothelial Dysfunctionmentioning

confidence: 77%

Section: Placental Ischemiamentioning

confidence: 78%

Section: Placental Ischemiamentioning

confidence: 99%

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Vascular Dysfunction in Preeclampsia

2014

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“…99 In pregnant rats with surgically induced reduced uterine blood flow, uterine resistance arteries had increased myogenic reactivity and decreased vasodilatory responses to methacholine and vascular endothelial growth factor. 100 Increased receptor-mediated uterine artery constriction has been also reported in models with experimental preeclampsia. Uterine arteries from the catechol-O-methyl transferase (COMT −/− ) knockout mouse 101,102 and the TgA rat (transgenic human angiotensinogen × human renin) exhibited augmented uterine artery responsiveness to phenylephrine and angiotensin II, respectively.…”

Section: Uterine Artery Functionmentioning

confidence: 96%

Maternal Vascular Physiology in Preeclampsia

Goulopoulou

2017

Hypertension

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“…This finding is consistent with enhanced myogenic reactivity in the reduced uteroplacental perfusion rat model of placental insufficiency. 27 Aged uterine arteries also had reduced maximum constrictor capacity-a well-described phenomenon in aging blood vessels. 28 Despite these changes in vasoconstrictor capacity of uterine arteries, vasodilator capacity was largely unchanged between young and aged dams during pregnancy.…”

Section: Advanced Maternal Age and Altered Uterine Artery Function Dumentioning

confidence: 98%

Effect of Advanced Maternal Age on Pregnancy Outcomes and Vascular Function in the Rat

et al. 2015

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Advanced maternal age is becoming increasingly common in Western societies and is associated with increased maternal and fetal morbidity and mortality. We hypothesized that aging results in impaired vascular function in pregnancy because of increased vascular oxidative stress and resultant scavenging of nitric oxide in both uterine and systemic arteries, causing reduced uteroplacental perfusion and poor pregnancy outcomes. Using aged rats (9.5 months), we investigated the effect of a delayed first natural pregnancy on pregnancy outcomes and uterine and mesenteric artery function on gestational day 20. Delayed pregnancy in the rat reduced fertility by 46%, reduced litter size by 36%, caused fetal growth restriction, increased placental weight, and increased maternal systolic blood pressure (by 16 mm Hg). Uterine arteries from aged dams displayed reduced constriction to phenylephrine (young: 14.3±0.94 mN/mm versus aged: 11.4±0.5 mN/mm, P =0.02) and potassium chloride (124 mmol/L; young: 21.8±1.27 mN/mm versus aged: 14.2±1.7 mN/mm; P =0.01). Methacholine-induced vasodilation was similar in uterine arteries from young and aged dams. However, mesenteric arteries from aged dams had a greater nitric oxide and a reduced endothelial-derived hyperpolarization contribution to methacholine-mediated vasodilation compared with young dams. Both uterine and mesenteric arteries from aged dams had greater active myogenic responses, with area under the curve increased by 228% and 151%, in aged uterine and mesenteric arteries, respectively. These results demonstrate that vascular function is altered at an advanced maternal age and provides further insights into the risks of poor pregnancy outcomes observed in women who delay pregnancy.

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Increased myogenic reactivity of uterine arteries from pregnant rats with reduced uterine perfusion pressure

Cited by 17 publications

References 32 publications

Vascular Dysfunction in Preeclampsia

Vascular Dysfunction in Preeclampsia

Maternal Vascular Physiology in Preeclampsia

Effect of Advanced Maternal Age on Pregnancy Outcomes and Vascular Function in the Rat

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