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Exercise-Induced Modulation of Angiotensin II Responses in Femoral Veins From 2-Kidney-1-Clip Hypertensive Rats

dc.contributor.authorChies, Agnaldo Bruno
dc.contributor.authorSpadella, Maria Angélica
dc.contributor.authorde Oliveira, Priscila Ramos
dc.contributor.authorDomeniconi, Raquel Fantin [UNESP]
dc.contributor.authorde Mello Santos, Talita [UNESP]
dc.contributor.authorMoreira, Roseli Peres
dc.contributor.authorRosales, Carla B.
dc.contributor.authorCasarini, Dulce Elena
dc.contributor.authorNavar, Luis Gabriel
dc.contributor.institutionMarília Medical School
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionTulane University School of Medicine
dc.date.accessioned2021-06-25T11:14:51Z
dc.date.available2021-06-25T11:14:51Z
dc.date.issued2021-04-07
dc.description.abstractThe present study investigated the angiotensin II (Ang II) responses in rat femoral veins taken from 2-kidney-1clip (2K1C) hypertensive rats at 4 weeks after clipping, as well as the effects of exercise on these responses. In this manner, femoral veins taken from 2K1C rats kept at rest or exposed to acute exercise or to exercise training were challenged with Ang II or endothelin-1 (ET-1) in organ bath. Simultaneously, the presence of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) were determined in these preparations by western blotting. In these experiments, femoral veins exhibited subdued Ang II responses. However, after nitric oxide (NO) synthesis blockade, the responses were higher in the femoral veins taken from animals kept at rest [0.137(0.049–0.245); n = 10] than those obtained in trained animals kept at rest [0.008(0.001–0.041); n = 10] or studied after a single bout of exercise [0.001(0.001–0.054); n = 11]. In preparations in which, in addition to NO synthesis, both the local production of prostanoids and the action of ET-1 on type A (ETA) or B (ETB) receptors were inhibited, the differences induced by exercise were no longer observed. In addition, neither ET-1 responses nor the presence of COX-1 and COX-2 in these preparations were modified by the employed exercise protocols. In conclusion, NO maintains Ang II responses reduced in femoral veins of 2K1C animals at rest. However, vasodilator prostanoids as well as other relaxing mechanisms, activated by ETB stimulation, are mobilized by exercise to cooperate with NO in order to maintain controlled Ang II responses in femoral veins.en
dc.description.affiliationLaboratory of Pharmacology Marília Medical School
dc.description.affiliationHuman Embryology Laboratory Marília Medical School
dc.description.affiliationDepartment of Anatomy Institute of Biociences UNESP
dc.description.affiliationDepartment of Medicine Nephrology Division Escola Paulista de Medicina Universidade Federal de São Paulo
dc.description.affiliationDepartment of Physiology and Hypertension and Renal Center of Excellence Tulane University School of Medicine
dc.description.affiliationUnespDepartment of Anatomy Institute of Biociences UNESP
dc.identifierhttp://dx.doi.org/10.3389/fphys.2021.620438
dc.identifier.citationFrontiers in Physiology, v. 12.
dc.identifier.doi10.3389/fphys.2021.620438
dc.identifier.issn1664-042X
dc.identifier.scopus2-s2.0-85104640722
dc.identifier.urihttp://hdl.handle.net/11449/208604
dc.language.isoeng
dc.relation.ispartofFrontiers in Physiology
dc.sourceScopus
dc.subject2K1C hypertension
dc.subjectangiotensin II
dc.subjectendothelin-1
dc.subjectexercise
dc.subjectfemoral vein
dc.subjectnitric oxide
dc.subjectprostanoids
dc.titleExercise-Induced Modulation of Angiotensin II Responses in Femoral Veins From 2-Kidney-1-Clip Hypertensive Ratsen
dc.typeArtigopt
dspace.entity.typePublication
relation.isOrgUnitOfPublicationab63624f-c491-4ac7-bd2c-767f17ac838d
relation.isOrgUnitOfPublication.latestForDiscoveryab63624f-c491-4ac7-bd2c-767f17ac838d
unesp.author.orcid0000-0001-9263-2475[1]
unesp.campusUniversidade Estadual Paulista (UNESP), Instituto de Biociências, Botucatupt
unesp.departmentAnatomia - IBBpt

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