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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...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9220223/ https://www.ncbi.nlm.nih.gov/pubmed/35740253 http://dx.doi.org/10.3390/biomedicines10061230 |
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author | Wangensteen, Rosemary Gómez-Guzmán, Manuel Banegas, Inmaculada Rodríguez-Gómez, Isabel Jiménez, Rosario Duarte, Juan García-Estañ, Joaquín Vargas, Félix |
author_facet | Wangensteen, Rosemary Gómez-Guzmán, Manuel Banegas, Inmaculada Rodríguez-Gómez, Isabel Jiménez, Rosario Duarte, Juan García-Estañ, Joaquín Vargas, Félix |
author_sort | Wangensteen, Rosemary |
collection | PubMed |
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. |
format | Online Article Text |
id | pubmed-9220223 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-92202232022-06-24 Vasoconstrictor and Pressor Effects of Des-Aspartate-Angiotensin I in Rat Wangensteen, Rosemary Gómez-Guzmán, Manuel Banegas, Inmaculada Rodríguez-Gómez, Isabel Jiménez, Rosario Duarte, Juan García-Estañ, Joaquín Vargas, Félix Biomedicines Article 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. MDPI 2022-05-25 /pmc/articles/PMC9220223/ /pubmed/35740253 http://dx.doi.org/10.3390/biomedicines10061230 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Wangensteen, Rosemary Gómez-Guzmán, Manuel Banegas, Inmaculada Rodríguez-Gómez, Isabel Jiménez, Rosario Duarte, Juan García-Estañ, Joaquín Vargas, Félix Vasoconstrictor and Pressor Effects of Des-Aspartate-Angiotensin I in Rat |
title | 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_short | Vasoconstrictor and Pressor Effects of Des-Aspartate-Angiotensin I in Rat |
title_sort | vasoconstrictor and pressor effects of des-aspartate-angiotensin i in rat |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9220223/ https://www.ncbi.nlm.nih.gov/pubmed/35740253 http://dx.doi.org/10.3390/biomedicines10061230 |
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