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. 2022 Jan 24:1–18. [Article in Spanish] doi: 10.1159/000521507

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Copyright © 2022 by S. Karger AG, Basel

This article is licensed under the Creative Commons Attribution 4.0 International License (CC BY). Usage, derivative works and distribution are permitted provided that proper credit is given to the author and the original publisher.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

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Fig. 4 — Esquema de la desregulación del SRAA mediada por la ACE2 en el COVID-19. El receptor de entrada a la célula huésped del SARS-CoV-2, ACE2, es un análogo de la ACE que participa en un paso clave en la regulación del SRAA: la conversión de Ang I en Ang II en el epitelio pulmonar. La Ang II actúa principalmente a través del receptor AT1. Alternativamente, la Ang II se metaboliza para producir angiotensina 1–7 (Ang 1–7), que actúa adicionalmente a través del Mas 1R. Fisiológicamente, el eje ACE/Ang II/AT1R se mantiene en equilibrio con el eje ACE2/Ang 1–7/Mas 1R. Al parecer, la unión del SARS-CoV-2 regula a la baja la señalización de la ACE2 y, en consecuencia, el eje ACE/Ang II/AT1R se impone, favoreciendo la constricción vascular, la inflamación en los tejidos y la fibrosis.