AT2 and MAS (but not AT1) angiotensinergic receptors in the medial amygdaloid nucleus modulate the baroreflex activity in rats

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dc.contributor.authorCosta-Ferreira, Willian [UNESP]
dc.contributor.authorGomes-de-Souza, Lucas [UNESP]
dc.contributor.authorCrestani, Carlos C. [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2019-10-06T15:51:50Z
dc.date.available2019-10-06T15:51:50Z
dc.date.issued2019-09-01
dc.description.abstractThe medial amygdaloid nucleus (MeA) is a limbic structure that has been demonstrated to be part of the central circuitry regulating baroreflex function. However, the local neurochemical mechanisms involved in baroreflex control by this forebrain structure is poorly understood. Thus, in the present study, we investigated the specific role of AT1, AT2, and MAS angiotensinergic receptors within the MeA in baroreflex responses in unanesthetized rats. For this, the baroreflex function was assessed using both the pharmacological approach via intravenous infusion of vasoactive agents and the sequence analysis technique. Using the pharmacological approach, we observed that bilateral microinjection of the selective AT2 receptor antagonist PD123319 into the MeA increased the tachycardia evoked by blood pressure decrease, but without affecting the reflex bradycardia caused by blood pressure increase. Besides, bilateral microinjection of the selective MAS receptor antagonist A-779 decreased both tachycardic and bradycardic responses of the baroreflex. The sequence analysis technique indicated that PD123319 into the MeA increased baroreflex effectiveness index while A-779 had an opposite effect. Treatment of the MeA with the selective AT1 receptor antagonist losartan did not affect baroreflex function assessed by either the pharmacological approach or sequence analysis technique. Overall, these findings provide evidence that MAS receptor within the MeA plays a facilitatory role in baroreflex function, whereas local AT2 receptor inhibits cardiac baroreflex responses. Results also indicate that AT1 receptor within the MeA is not involved in the control of baroreflex function.en
dc.description.affiliationLaboratory of Pharmacology School of Pharmaceutical Sciences São Paulo State University (UNESP), Rodovia Araraquara-Jaú Km 01 (Campus Universitário), Campus Ville
dc.description.affiliationJoint UFSCar-UNESP Graduate Program in Physiological Sciences
dc.description.affiliationUnespLaboratory of Pharmacology School of Pharmaceutical Sciences São Paulo State University (UNESP), Rodovia Araraquara-Jaú Km 01 (Campus Universitário), Campus Ville
dc.description.affiliationUnespJoint UFSCar-UNESP Graduate Program in Physiological Sciences
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipIdFAPESP: 2015/05922-9
dc.description.sponsorshipIdFAPESP: 2017/19249-0
dc.description.sponsorshipIdCNPq: 304108/2018-9
dc.description.sponsorshipIdCNPq: 456405/2014-3
dc.format.extent1173-1182
dc.identifierhttp://dx.doi.org/10.1007/s00424-019-02301-3
dc.identifier.citationPflugers Archiv European Journal of Physiology, v. 471, n. 9, p. 1173-1182, 2019.
dc.identifier.doi10.1007/s00424-019-02301-3
dc.identifier.issn1432-2013
dc.identifier.issn0031-6768
dc.identifier.scopus2-s2.0-85070293451
dc.identifier.urihttp://hdl.handle.net/11449/187935
dc.language.isoeng
dc.relation.ispartofPflugers Archiv European Journal of Physiology
dc.rights.accessRightsAcesso aberto
dc.sourceScopus
dc.subjectA-779
dc.subjectAmygdala
dc.subjectAT2 receptor
dc.subjectBlood pressure
dc.subjectHeart rate
dc.subjectLosartan
dc.subjectMAS receptor
dc.subjectPD123319
dc.titleAT2 and MAS (but not AT1) angiotensinergic receptors in the medial amygdaloid nucleus modulate the baroreflex activity in ratsen
dc.typeArtigo
unesp.author.lattes1117432571971568[3]
unesp.author.orcid0000-0002-1942-858X[3]

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