dc.contributor |
Háskóli Íslands |
dc.contributor |
University of Iceland |
dc.contributor.author |
Helgadottir, Helga |
dc.contributor.author |
Tropea, Teresa |
dc.contributor.author |
Gizurarson, Sveinbjorn |
dc.contributor.author |
Meiri, Hamutal |
dc.contributor.author |
Mandalà, Maurizio |
dc.date.accessioned |
2020-10-13T14:36:27Z |
dc.date.available |
2020-10-13T14:36:27Z |
dc.date.issued |
2019-01 |
dc.identifier.citation |
Helgadottir, H., et al. (2019). "Aspirin causes endothelium-dependent vasodilation of resistance arteries from non-gravid and gravid rats." Pregnancy Hypertension 15: 141-145. |
dc.identifier.issn |
2210-7789 |
dc.identifier.uri |
https://hdl.handle.net/20.500.11815/2116 |
dc.description |
Publisher's version (útgefin grein) |
dc.description.abstract |
Objective:Theobjectiveofthisstudywastounderstandtheeffectofacetylsalicylicacid(aspirin)onresistancearteriesfrommesenteryanduterus.Duringpregnancy,the uterine vasculature undergoes consistent growth to provide sufficient uteroplacental blood flow, a process whose failure is associated with pregnancy compli-cations characterized by high uterine vascular resistance.Methods:Uterine arcuate (UA) and mesenteric arteries (MA; diameter<300μm) isolated from non-gravid, mid-gravid (day 14), and late-gravid rats (day 20) wereexposedtoaspirin(10−12to10−5M).Further,inUAfromlate-gravidrats,aspirinwasevaluatedinpresenceofinhibitorsofnitricoxidesynthases,cyclooxygenase,cyclic nucleotides (cAMP, cGMP) and BK channels, and also on endothelium-denuded vessels.Results:Aspirin dilated both UA and MA in a dose dependent manner. Pregnancy increased aspirin vasodilation in MA and UA from mid-gravid rats, an effect thatwas reduced in vessels from late gravid animals at concentrations>10−7M. Further, uterine vasodilation was significantly reduced when the endothelium wasremoved (p < 0.001), and by inhibitors of nitric oxide synthase (p < 0.001), cyclooxygenase synthase (p < 0.05), cyclic nucleotides cGMP/cAMP and BKchannels.Conclusion:This is the first study to show a direct vasodilatory effect of aspirin on rat uterine artery that is mediated by a combination of cellular – primarilyendothelial - mechanisms. Our results in UA suggest that the use of aspirin may be effective in enhancing uteroplacental blood flow,while its vasodilation effect onMA may lower peripheral resistance. |
dc.description.sponsorship |
This study was supported by grants from the European Union 7th Framework Programme – FP7-HEALTH-2013-INNOVATION-2 (ASPRE Project # 601852), Hananja ehf, and by the Icelandic Research Fund. |
dc.format.extent |
141-145 |
dc.language.iso |
en |
dc.publisher |
Elsevier BV |
dc.relation |
info:eu-repo/grantAgreement/EC/FP7/601852 |
dc.relation.ispartofseries |
Pregnancy Hypertension;15 |
dc.rights |
info:eu-repo/semantics/openAccess |
dc.subject |
Aspirin |
dc.subject |
Endothelium-dependent |
dc.subject |
Mesentery |
dc.subject |
Uterus |
dc.subject |
Verkjalyf |
dc.subject |
Meðganga |
dc.subject |
Leg |
dc.title |
Aspirin causes endothelium-dependent vasodilation of resistance arteries from non-gravid and gravid rats |
dc.type |
info:eu-repo/semantics/article |
dcterms.license |
This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/BY-NC-ND/4.0/). |
dc.description.version |
Peer Reviewed |
dc.identifier.journal |
Pregnancy Hypertension |
dc.identifier.doi |
10.1016/j.preghy.2019.01.001 |
dc.relation.url |
https://www.sciencedirect.com/science/article/pii/S2210778918300370 |
dc.contributor.department |
Lyfjafræðideild (HÍ) |
dc.contributor.department |
Faculty of Pharmaceutical Sciences (UI) |
dc.contributor.school |
Heilbrigðisvísindasvið (HÍ) |
dc.contributor.school |
School of Health Sciences (UI) |