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dc.contributor.authorMarshall, SA
dc.contributor.authorSenadheera, SN
dc.contributor.authorJelinic, M
dc.contributor.authorO'Sullivan, K
dc.contributor.authorParry, LJ
dc.contributor.authorTare, M
dc.date.accessioned2020-12-17T03:05:18Z
dc.date.available2020-12-17T03:05:18Z
dc.date.issued2018-03-22
dc.identifier.citationMarshall, S. A., Senadheera, S. N., Jelinic, M., O'Sullivan, K., Parry, L. J. & Tare, M. (2018). Relaxin Deficiency Leads to Uterine Artery Dysfunction During Pregnancy in Mice. FRONTIERS IN PHYSIOLOGY, 9 (MAR), https://doi.org/10.3389/fphys.2018.00255.
dc.identifier.issn1664-042X
dc.identifier.urihttp://hdl.handle.net/11343/254738
dc.description.abstractThe 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.
dc.languageEnglish
dc.publisherFRONTIERS MEDIA SA
dc.titleRelaxin Deficiency Leads to Uterine Artery Dysfunction During Pregnancy in Mice
dc.typeJournal Article
dc.identifier.doi10.3389/fphys.2018.00255
melbourne.affiliation.departmentUniversity General
melbourne.affiliation.departmentSchool of BioSciences
melbourne.source.titleFrontiers in Physiology
melbourne.source.volume9
melbourne.source.issueMAR
dc.rights.licenseCC BY
melbourne.elementsid1319438
melbourne.contributor.authorParry, Laura
melbourne.contributor.authorMarshall, Sarah
dc.identifier.eissn1664-042X
melbourne.accessrightsOpen Access


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