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      Sistema renina-angiotensina (SRA) en las patologías cardiovasculares: papel sobre la hipertensión arterial Translated title: Renin-angiotensin system (RAS) in cardiovascular pathologies: role on arterial hypertension

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          Abstract

          Resumen Introducción. En las patologías cardiovasculares como insuficiencia cardiaca, hipertensión arterial, vasculopatías, enfermedades coronarias, etc; el sistema renina-angiotensina (SRA) tiene participación clave, cuyas acciones principales incluyen la regulación de la presión arterial, el tono vascular, la volemia y facilitar la transmisión simpática. Objetivo. En este ensayo se discuten estos aspectos del SRA como resultado de una secuencia de transformaciones de distintas proteínas, comenzando por la acción de la renina que transforma el angiotensinógeno en angiotensina-I y posteriormente, este se convierte en angiotensina II por acción de la enzima convertidora de angiotensina I (ECA I). Conclusiones. Cuando este sistema se ve alterado culmina en hipertensión arterial, la cual se puede controlar mediante tratamientos farmacológicos empleando inhibidores químicos cuyos mecanismos de acción se basan en impedir que estas enzimas se unan a su sustrato y así se mantenga un equilibrio homeostático en la presión arterial.

          Translated abstract

          Abstract Introduction. In cardiovascular pathologies such as heart failure, arterial hypertension, vasculopathies, coronary diseases, etc; the renin-angiotensin system (RAS) has an essential role. The main actions include the regulation of blood pressure, vascular tone, volemia and facilitating sympathetic transmission. Objective. This manuscript summarizes these aspects of the SRA and discussed the sequence of transformations of different proteins, beginning with the action of renin that transforms the angiotensinogen into angiotensin-I and later, it is converted into angiotensin II by the action of the Angiotensin-I converting enzyme (ACE-I). Conclusions. When this system is altered culminates in hypertension, which can be controlled by pharmacological treatments using chemical inhibitors whose action mechanisms are based on preventing these enzymes from binding to their substrate and thus maintain a homeostatic balance in the pressure arterial.

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          The renin‐angiotensin‐aldosterone system and its suppression

          Chronic activation of the renin‐angiotensin‐aldosterone system (RAAS) promotes and perpetuates the syndromes of congestive heart failure, systemic hypertension, and chronic kidney disease. Excessive circulating and tissue angiotensin II (AngII) and aldosterone levels lead to a pro‐fibrotic, ‐inflammatory, and ‐hypertrophic milieu that causes remodeling and dysfunction in cardiovascular and renal tissues. Understanding of the role of the RAAS in this abnormal pathologic remodeling has grown over the past few decades and numerous medical therapies aimed at suppressing the RAAS have been developed. Despite this, morbidity from these diseases remains high. Continued investigation into the complexities of the RAAS should help clinicians modulate (suppress or enhance) components of this system and improve quality of life and survival. This review focuses on updates in our understanding of the RAAS and the pathophysiology of AngII and aldosterone excess, reviewing what is known about its suppression in cardiovascular and renal diseases, especially in the cat and dog.
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            Tissue renin-angiotensin-aldosterone systems: Targets for pharmacological therapy.

            The renin-angiotensin-aldosterone system is one of the most important systems in cardiovascular control and in the pathogenesis of cardiovascular diseases. Therefore, it is already a very successful drug target for the therapy of these diseases. However, angiotensins are generated not only in the plasma but also locally in tissues from precursors and substrates either locally expressed or imported from the circulation. In most areas of the brain, only locally generated angiotensins can exert effects on their receptors owing to the blood-brain barrier. Other tissue renin-angiotensin-aldosterone systems are found in cardiovascular organs such as kidney, heart, and vessels and play important roles in the function of these organs and in the deleterious actions of hypertension and diabetes on these tissues. Novel components with mostly opposite actions to the classical renin-angiotensin-aldosterone systems have been described and need functional characterization to evaluate their suitability as novel drug targets.
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              Three key proteases – angiotensin-I-converting enzyme (ACE), ACE2 and renin – within and beyond the renin-angiotensin system

              Summary The discovery of angiotensin-I-converting enzyme 2 (ACE2) and a (pro)renin receptor has renewed interest in the physiology of the renin-angiotensin system (RAS). Through the ACE2/angiotensin-(1–7)/Mas counter-regulatory axis, ACE2 balances the vasoconstrictive, proliferative, fibrotic and proinflammatory effects of the ACE/angiotensin II/AT1 axis. The (pro)renin receptor system shows an angiotensin-dependent function related to increased generation of angiotensin I, and an angiotensin-independent aspect related to intracellular signalling. Activation of ACE2 and inhibition of ACE and renin have been at the core of the RAS regulation. The aim of this review is to discuss the biochemistry and biological functions of ACE, ACE2 and renin within and beyond the RAS, and thus provide a perspective for future bioactives from natural plant and/or food resources related to the three proteases.
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                Author and article information

                Journal
                jonnpr
                Journal of Negative and No Positive Results
                JONNPR
                Research and Science S.L. (Madrid, Madrid, Spain )
                2529-850X
                2021
                : 6
                : 1
                : 163-176
                Affiliations
                [1] Mérida Yucatán orgnameUniversidad Autónoma de Yucatán orgdiv1Facultad de Ingeniería Química Mexico
                Article
                S2529-850X2021000100010 S2529-850X(21)00600100010
                10.19230/jonnpr.3712
                05d0ddb9-cc1b-40c9-adf7-96bab5e33be7

                This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.

                History
                : 30 April 2020
                : 16 August 2020
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 16, Pages: 14
                Product

                SciELO Spain

                Categories
                Revisión

                inhibidores,Angiotensin,hypertension,inhibitors,Renina,Angiotensina,hipertensión,Renin

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