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Vasoconstrictor and Pressor Effects of Des-Aspartate-Angiotensin I in Rat.

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dc.archivorevisadoDuarte, Juan
dc.contributor.authorGarcia-estañ Lopez, J. M.
dc.contributor.authorWangensteen,Rosemary
dc.contributor.authorGómez-Guzmán, Manuel
dc.contributor.authorBanegas, Inmaculada
dc.contributor.authorRodríguez-Gómez, Isabel
dc.contributor.authorJiménez, Rosario
dc.contributor.authorVargas,Félix
dc.contributor.authorDuarte, Juan
dc.contributor.departmentFisiología
dc.date.accessioned2023-09-21T22:10:58Z
dc.date.available2023-09-21T22:10:58Z
dc.date.issued2022-05-22
dc.description© 2023 The Authors. This document is made available under the CC-BY-NC 4.0 license http://creativecommons.org/licenses/by-nc /4.0/ This document is the Accepted version of a Published Work that appeared in final form in Biomedicines. To access the final edited and published work see https://doi.org/10.3390/biomedicines10061230
dc.description.abstractThis study investigated the vasoactive effects of des-aspartate-angiotensin-I (DAA-I) in male Wistar rats on whole body vascular bed, isolated perfused kidneys, and aortic rings. Dose– response curves to DAA-I were compared with those to angiotensin II (Ang II). The Ang II-type-1 (AT1) receptor blocker, losartan, was used to evaluate the role of AT1 receptors in the responses to DAA-I. Studies were also conducted of the responsiveness in aortic rings after endotheliumremoval, nitric oxide synthase inhibition, or AT2 receptor blockade. DAA-I induced a dose-related systemic pressor response that was shifted to the right compared with Ang II. Losartan markedly attenuated the responsiveness to DAA-I. DAA-I showed a similar pattern in renal vasculature and aortic rings. In aortic rings, removal of endothelium and nitric oxide inhibition increased the sensitivity and maximal response to DAA-I and Ang II. AT2 receptor blockade did not significantly affect the responsiveness to DAA-I. According to these findings, DAA-I increases the systemic blood pressure and vascular tone in conductance and resistance vessels via AT1 receptor activation. This vasoconstrictor effect of DAA-I participates in the homeostatic control of arterial pressure, which can also contribute to the pathogenesis of hypertension. DAA-I may therefore be a potential therapeutic target in cardiovascular disease.
dc.formatapplication/pdfes_ES
dc.format.extent12
dc.identifier.citationBiomedicines 2022, 10, 1230
dc.identifier.issn2227-9059
dc.identifier.urihttp://hdl.handle.net/10201/134130
dc.languageenges_ES
dc.relation.isreferencedbyED_IDENTRADA=1168
dc.rightsinfo:eu-repo/semantics/openAccess*
dc.rightsAtribución 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectRatses_ES
dc.subjectAngiotensin Ies_ES
dc.subjectRenin-angiotensin system
dc.subjectDes-aspartate-angiotensin I
dc.subjectVascular reactivity
dc.subjectKidney
dc.subjectHypertension
dc.titleVasoconstrictor and Pressor Effects of Des-Aspartate-Angiotensin I in Rat.es_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dspace.entity.typePublicationes
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