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dc.contributor.authorHelgadóttir, Helga; email: helgadottir@hi.is
dc.contributor.authorTropea, Teresa; email: teresa.tropea@manchester.ac.uk
dc.contributor.authorGizurarson, Sveinbjörn; orcid: 0000-0001-7824-9752; email: sveinbj@hi.is
dc.contributor.authorMandalà, Maurizio; orcid: 0000-0003-3736-0205; email: m.mandala@unical.it
dc.date.accessioned2021-09-23T00:23:36Z
dc.date.available2021-09-23T00:23:36Z
dc.date.issued2021-09-21
dc.identifierhttps://chesterrep.openrepository.com/bitstream/handle/10034/625910/additional-files.zip?sequence=2
dc.identifierhttps://chesterrep.openrepository.com/bitstream/handle/10034/625910/ijms-22-10162.xml?sequence=3
dc.identifierhttps://chesterrep.openrepository.com/bitstream/handle/10034/625910/ijms-22-10162.pdf?sequence=4
dc.identifier.citationInternational Journal of Molecular Sciences, volume 22, issue 18, page e10162
dc.identifier.urihttp://hdl.handle.net/10034/625910
dc.descriptionFrom MDPI via Jisc Publications Router
dc.descriptionHistory: accepted 2021-09-16, pub-electronic 2021-09-21
dc.descriptionPublication status: Published
dc.descriptionFunder: Seventh Framework Programme; Grant(s): 601852
dc.descriptionFunder: Icelandic Research Fund; Grant(s): 163369-051
dc.description.abstractAcetylsalicylic acid (aspirin) exhibits a broad range of activities, including analgesic, antipyretic, and antiplatelet properties. Recent clinical studies also recommend aspirin prophylaxis in women with a high risk of pre-eclampsia, a major complication of pregnancy characterized by hypertension. We investigated the effect of aspirin on mesenteric resistance arteries and found outdiscovered the molecular mechanism underlying this action. Aspirin (10−12–10−6 M) was tested on pregnant rat mesenteric resistance arteries by a pressurized arteriography. Aspirin was investigated in the presence of several inhibitors of: (a) nitric oxide synthase (L-NAME 2 × 10−4 M); (b) cyclooxygenase (Indomethacin, 10−5 M); (c) Ca2+-activated K+ channels (Kca): small conductance (SKca, Apamin, 10−7 M), intermediate conductance (IKca, TRAM34, 10−5 M), and big conductance (BKca, paxilline, 10−5 M); and (d) endothelial-derived hyperpolarizing factor (high KCl, 80 mM). Aspirin caused a concentration-dependent vasodilation. Aspirin-vasodilation was abolished by removal of endothelium or by high KCl. Furthermore, preincubation with either apamin plus TRAM-34 or paxillin significantly attenuated aspirin vasodilation (p 0.05). For the first time, we showed that aspirin induced endothelium-dependent vasodilation in mesenteric resistance arteries through the endothelial-derived hyperpolarizing factor (EDHF) and calcium-activated potassium channels. By activating this molecular mechanism, aspirin may lower peripheral vascular resistance and be beneficial in pregnancies complicated by hypertension.
dc.languageen
dc.publisherMDPI
dc.rightsLicence for this article: https://creativecommons.org/licenses/by/4.0/
dc.sourceeissn: 1422-0067
dc.subjectendothelial cells
dc.subjectsmooth muscle cells
dc.subjectrelaxation
dc.subjectpre-eclampsia
dc.subjecthypertension
dc.subjectcalcium-activated potassium channels
dc.titleEndothelium-Derived Hyperpolarizing Factor (EDHF) Mediates Acetylsalicylic Acid (Aspirin) Vasodilation of Pregnant Rat Mesenteric Arteries
dc.typearticle
dc.date.updated2021-09-23T00:23:36Z
dc.date.accepted2021-09-16


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