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Relaxin Deficiency Leads to Uterine Artery Dysfunction During Pregnancy in Mice

Overview of attention for article published in Frontiers in Physiology, March 2018
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Title
Relaxin Deficiency Leads to Uterine Artery Dysfunction During Pregnancy in Mice
Published in
Frontiers in Physiology, March 2018
DOI 10.3389/fphys.2018.00255
Pubmed ID
Authors

Sarah A. Marshall, Sevvandi N. Senadheera, Maria Jelinic, Kelly O'Sullivan, Laura J. Parry, Marianne Tare

Abstract

The uterine vasculature undergoes profound adaptations in response to pregnancy. Augmentation of endothelial vasodilator function and reduced smooth muscle reactivity are factors contributing to uterine artery adaptation and are critical for adequate placental perfusion. The peptide hormone relaxin has an important role in mediating the normal maternal renal vascular adaptations during pregnancy through a reduction in myogenic tone and an increase in flow-mediated vasodilation. Little is known however about the influence of endogenous relaxin on the uterine artery during pregnancy. We tested the hypothesis that relaxin deficiency increases myogenic tone and impairs endothelial vasodilator function in uterine arteries of late pregnant relaxin deficient (Rln-/-) mice. Reactivity of main uterine arteries from non-pregnant and late pregnant wild-type (Rln+/+) and Rln-/- mice was studied using pressure and wire myography and changes in gene expression explored using PCR. Myogenic tone was indistinguishable in arteries from non-pregnant mice. In late pregnancy uterine artery myogenic tone was halved in Rln+/+ mice (P < 0.0001), an adaptation that failed to occur in arteries from pregnant Rln-/- mice. The role of vasodilator prostanoids in the regulation of myogenic tone was significantly reduced in arteries of pregnant Rln-/- mice (P = 0.02). Agonist-mediated endothelium-dependent vasodilation was significantly impaired in non-pregnant Rln-/- mice. With pregnancy, differences in total endothelial vasodilator function were resolved, although there remained an underlying deficiency in the role of vasodilator prostanoids and alterations to the contributions of calcium-activated K+ channels. Fetuses of late pregnant Rln-/- mice were ~10% lighter (P < 0.001) than those of Rln+/+ mice. In conclusion, relaxin deficiency is associated with failed suppression of uterine artery myogenic tone in pregnancy, which likely contributes to reduced uteroplacental perfusion and fetal growth restriction.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 26 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 26 100%

Demographic breakdown

Readers by professional status Count As %
Student > Bachelor 5 19%
Student > Master 5 19%
Student > Ph. D. Student 3 12%
Other 2 8%
Student > Postgraduate 2 8%
Other 2 8%
Unknown 7 27%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 4 15%
Medicine and Dentistry 3 12%
Nursing and Health Professions 2 8%
Agricultural and Biological Sciences 2 8%
Pharmacology, Toxicology and Pharmaceutical Science 1 4%
Other 4 15%
Unknown 10 38%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 29 March 2018.
All research outputs
#20,472,403
of 23,031,582 outputs
Outputs from Frontiers in Physiology
#9,488
of 13,775 outputs
Outputs of similar age
#293,590
of 332,503 outputs
Outputs of similar age from Frontiers in Physiology
#305
of 420 outputs
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