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

This 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 block...

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Autores: Wangensteen, Rosemary, Gómez-Guzmán, Manuel, Banegas, Inmaculada, Rodríguez-Gómez, Isabel, Jiménez-Moleón, Rosario, Duarte, Juan, García-Estaño, Joaquín, Vargas, Félix
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2022
País:España
Institución:Universidad de Jaén
Repositorio:RUJA. Repositorio Institucional de la Producción Científica de la Universidad de Jaén
OAI Identifier:oai:ruja.ujaen.es:10953/2313
Acceso en línea:https://hdl.handle.net/10953/2313
Access Level:acceso abierto
Palabra clave:Des-aspartate-angiotensin I
Hypertension
Kidney
Renin-angiotensin system
Vascular reactivity
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spelling Vasoconstrictor and Pressor Effects of Des-Aspartate-Angiotensin I in RatWangensteen, RosemaryGómez-Guzmán, ManuelBanegas, InmaculadaRodríguez-Gómez, IsabelJiménez-Moleón, RosarioDuarte, JuanGarcía-Estaño, JoaquínVargas, FélixDes-aspartate-angiotensin IHypertensionKidneyRenin-angiotensin systemVascular reactivityThis 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 endothelium removal, 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.MDPI202420242022info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://hdl.handle.net/10953/2313reponame:RUJA. Repositorio Institucional de la Producción Científica de la Universidad de Jaéninstname:Universidad de JaénInglésBIOMEDICINES 10 (6)1230CC0 1.0 Universalhttp://creativecommons.org/publicdomain/zero/1.0/info:eu-repo/semantics/openAccessoai:ruja.ujaen.es:10953/23132026-06-24T12:41:07Z
dc.title.none.fl_str_mv Vasoconstrictor and Pressor Effects of Des-Aspartate-Angiotensin I in Rat
title Vasoconstrictor and Pressor Effects of Des-Aspartate-Angiotensin I in Rat
spellingShingle Vasoconstrictor and Pressor Effects of Des-Aspartate-Angiotensin I in Rat
Wangensteen, Rosemary
Des-aspartate-angiotensin I
Hypertension
Kidney
Renin-angiotensin system
Vascular reactivity
title_short Vasoconstrictor and Pressor Effects of Des-Aspartate-Angiotensin I in Rat
title_full Vasoconstrictor and Pressor Effects of Des-Aspartate-Angiotensin I in Rat
title_fullStr Vasoconstrictor and Pressor Effects of Des-Aspartate-Angiotensin I in Rat
title_full_unstemmed Vasoconstrictor and Pressor Effects of Des-Aspartate-Angiotensin I in Rat
title_sort Vasoconstrictor and Pressor Effects of Des-Aspartate-Angiotensin I in Rat
dc.creator.none.fl_str_mv Wangensteen, Rosemary
Gómez-Guzmán, Manuel
Banegas, Inmaculada
Rodríguez-Gómez, Isabel
Jiménez-Moleón, Rosario
Duarte, Juan
García-Estaño, Joaquín
Vargas, Félix
author Wangensteen, Rosemary
author_facet Wangensteen, Rosemary
Gómez-Guzmán, Manuel
Banegas, Inmaculada
Rodríguez-Gómez, Isabel
Jiménez-Moleón, Rosario
Duarte, Juan
García-Estaño, Joaquín
Vargas, Félix
author_role author
author2 Gómez-Guzmán, Manuel
Banegas, Inmaculada
Rodríguez-Gómez, Isabel
Jiménez-Moleón, Rosario
Duarte, Juan
García-Estaño, Joaquín
Vargas, Félix
author2_role author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Des-aspartate-angiotensin I
Hypertension
Kidney
Renin-angiotensin system
Vascular reactivity
topic Des-aspartate-angiotensin I
Hypertension
Kidney
Renin-angiotensin system
Vascular reactivity
description This 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 endothelium removal, 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.
publishDate 2022
dc.date.none.fl_str_mv 2022
2024
2024
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv https://hdl.handle.net/10953/2313
url https://hdl.handle.net/10953/2313
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv BIOMEDICINES 10 (6)1230
dc.rights.none.fl_str_mv CC0 1.0 Universal
http://creativecommons.org/publicdomain/zero/1.0/
info:eu-repo/semantics/openAccess
rights_invalid_str_mv CC0 1.0 Universal
http://creativecommons.org/publicdomain/zero/1.0/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv MDPI
publisher.none.fl_str_mv MDPI
dc.source.none.fl_str_mv reponame:RUJA. Repositorio Institucional de la Producción Científica de la Universidad de Jaén
instname:Universidad de Jaén
instname_str Universidad de Jaén
reponame_str RUJA. Repositorio Institucional de la Producción Científica de la Universidad de Jaén
collection RUJA. Repositorio Institucional de la Producción Científica de la Universidad de Jaén
repository.name.fl_str_mv
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