Publication:
[Pyr1]apelin-13 relaxes the rat thoracic aorta via APJ, NO, AMPK, and potassium channels

dc.contributor.authorŞahintürk, Serdar
dc.contributor.authorDemirel, Sadettin
dc.contributor.authorÖzyener, Fadıl
dc.contributor.authorİşbil, Naciye
dc.contributor.buuauthorŞAHİNTÜRK, SERDAR
dc.contributor.buuauthorDEMİREL, SADETTİN
dc.contributor.buuauthorÖZYENER, FADIL
dc.contributor.buuauthorİŞBİL, NACİYE
dc.contributor.departmentBursa Uludağ Üniversitesi/Tıp Fakültesi/Fizyoloji Anabilim Dalı
dc.contributor.orcid0000-0002-7612-0055
dc.contributor.orcid0000-0002-3629-5344
dc.contributor.orcid0000-0002-4606-6596
dc.contributor.researcheridAAH-3460-2021
dc.contributor.researcheridACQ-9887-2022
dc.contributor.researcheridAAH-1641-2021
dc.contributor.researcheridFBW-7104-2022
dc.date.accessioned2024-06-25T05:41:48Z
dc.date.available2024-06-25T05:41:48Z
dc.date.issued2021-01-01
dc.description.abstractIn this study, the effect and effect mechanisms of [Pyr1]apelin-13, the dominant apelin isoform in the human cardiovascular tissues and human plasma, on vascular contractility were investigated. The vascular rings obtained from the thoracic aortas of the male Wistar Albino rats were placed in the isolated tissue bath system. After the equilibration period, [Pyr1]apelin-13 (10(-9) to 10(-6) M) was applied cumulatively to the aortic rings pre-contracted with phenylephrine in the plateau phase. The protocol was repeated in the presence of specific signaling pathway inhibitors (F13A, L-NAME, dorsomorphin, TEA, U0126, or indomethacin) to determine the effect mechanisms of [Pyr1]apelin-13. [Pyr1]apelin-13 induced a dose-dependent relaxation in the pre-contracted aortic rings. APJ, eNOS, AMPK, and potassium channel inhibition statistically significantly decreased the vasodilator effect of [Pyr1]apelin-13. MAPK and COX inhibition didn't statistically significantly changed the vasodilator effect of [Pyr1]apelin-13. In conclusion, [Pyr1]apelin-13 relaxes the rat thoracic aorta via APJ, NO, AMPK, and potassium channels.
dc.identifier.doi10.4149/gpb_2021028
dc.identifier.eissn1338-4325
dc.identifier.endpage434
dc.identifier.issn0231-5882
dc.identifier.issue5
dc.identifier.startpage427
dc.identifier.urihttps://doi.org/10.4149/gpb_2021028
dc.identifier.urihttps://www.elis.sk/index.php
dc.identifier.urihttps://hdl.handle.net/11452/42310
dc.identifier.volume40
dc.identifier.wos000704283000008
dc.indexed.wosWOS.SCI
dc.language.isoen
dc.publisherAepress Sro
dc.relation.journalGeneral Physiology and Biophysics
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi
dc.relation.tubitak119S971
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectActivated protein-kinase
dc.subjectBlood-pressure
dc.subjectApelin
dc.subjectElabela/toddler
dc.subjectMechanisms
dc.subjectArteries
dc.subject[pyr1]apelin-13
dc.subjectAmpk
dc.subjectApj
dc.subjectNo
dc.subjectPotassium channels
dc.subjectScience & technology
dc.subjectLife sciences & biomedicine
dc.subjectBiochemistry & molecular biology
dc.subjectBiophysics
dc.subjectPhysiology
dc.title[Pyr1]apelin-13 relaxes the rat thoracic aorta via APJ, NO, AMPK, and potassium channels
dc.typeArticle
dspace.entity.typePublication
relation.isAuthorOfPublication25bede72-9942-49c8-b45d-1e94eaf9062d
relation.isAuthorOfPublicationbf421fa5-e949-4453-b2b2-c4a9df1be392
relation.isAuthorOfPublication4c0e0603-772f-4429-b7ca-9d8e68702800
relation.isAuthorOfPublication6459c031-8ea7-4356-91ed-9d11cffa5a69
relation.isAuthorOfPublication.latestForDiscovery25bede72-9942-49c8-b45d-1e94eaf9062d

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