Interação entre SARS-COV-2 e o sistema Renina Angiotensina

Abstract

A mortalidade ocasionada pela SARS-CoV-2 está associada aos seguintes fatores: Diabetes Mellitus, Hipertensão Arterial Sistêmica (HAS), Doença Arterial Coronariana e idade acima de 70 anos (único fator não modificável) 5 . O processo inflamatório apresenta também associação com a mortalidade após infecção pela SARS-CoV-2. Marcadores inflamatórios elevados, como Proteína C Reativa e Interleucina-6, foram preditores de pior prognóstico 1 .De acordo com a fisiopatologia descrita até então, a SARS-CoV-2 penetra nas células humanas pelos mesmos receptores da Enzima Conversora de Angiotensina 2 (ECA 2). A ECA 2 é uma enzima constituinte do Sistema Renina-Angiotensina (SRA), sendo expressa principalmente no endotélio arterial das coronárias e vasos intra-renais, no tecido epitelial pulmonar e enterócitos [6][7] . O entendimento da interação da SARS-CoV-2 com o SRA é de grande importância para atuação dos mais diferentes profissionais de saúde. Portanto, neste artigo objetivamos descrever com profundidade o SRA e posteriormente a interação entre a SARS-CoV-2 com esse sistema. Dessa forma, procuramos elucidar algumas questões ainda pouco compreendidas sobre a enfermidade e levantamos algumas hipóteses baseadas no contexto exposto que poderão nortear futuras investigações. Sistema Renina AngiotensinaO SRA pode ser dividido em sistêmico e tecidual. A produção de angiotensinas que agem nos diferentes tecidos corporais (SRA sistêmico) tem como protagonistas o fígado, os rins e o endotélio vascular arterial, tratando-se de um sistema hormonal endócrino. Já o SRA tecidual age de forma autócrina e parácrina. Todos os constituintes do SRA são produzidos de forma local no coração, cérebro, vasos sanguíneos arteriais (endotélio), rins, glândulas adrenais, órgãos reprodutores, pâncreas e tecido adiposo [7][8][9] . Como os SRA sistêmico e tecidual são homólogos, iremos descrever especificamente a via sistêmica, nos reportando quando necessário, à via tecidual.

Renin-Angiotensin-Aldosterone System in Women Using Combined Oral Contraceptive: A Systematic Review

“…The decrease in renin concentration is justified by an increase in the levels of angiotensin II that decreases the production of renin through negative feedback, determining the balance of this system. 23 Despite this, the study developed by our research group found a median 2-fold higher renin concentration in women who use COC compared with women who do not. 7 The reasons that justify this opposition between the aforementioned studies are unknown.…”

“…23 Aldosterone is a mineralocorticoid, which by binding to the mineralocorticoid receptor on the epithelial cells, recruits sodium channels to the surface of renal epithelial cells, increasing sodium reabsorption, potassium excretion, and plasma volume expansion, culminating in BP elevation. 23 In a literature review carried out in 1996, COCs with high doses of EE (>30mcg) were identified as precursors of SAH, noting a high sodium retention effect in this population. 5 In this regard, so-called low-dose COCs ( 30 mcg of EE) have been formulated in an attempt to decrease the effects of EE on sodium retention.…”

“…It exerts its actions on target organs and can act by means of conversion into other molecules (angiotensin I–VII, angiotensin I–IX, or angiotensin III) or by binding to its AT1 and AT2 receptors. 23 24 In isolation, angiotensin II has the potential to stimulate the production of antidiuretic hormone, increase the reabsorption of sodium in the kidneys, stimulate sympathetic activity, and trigger direct vasoconstriction of the arterial vessels by binding to AT1 receptors, favoring the elevation of BP. 23 Additionally, when angiotensin II is converted to angiotensin III, it induces the production of aldosterone by the adrenals which will also act mainly on the kidneys.…”

“… 23 24 In isolation, angiotensin II has the potential to stimulate the production of antidiuretic hormone, increase the reabsorption of sodium in the kidneys, stimulate sympathetic activity, and trigger direct vasoconstriction of the arterial vessels by binding to AT1 receptors, favoring the elevation of BP. 23 Additionally, when angiotensin II is converted to angiotensin III, it induces the production of aldosterone by the adrenals which will also act mainly on the kidneys. 23 Aldosterone is a mineralocorticoid, which by binding to the mineralocorticoid receptor on the epithelial cells, recruits sodium channels to the surface of renal epithelial cells, increasing sodium reabsorption, potassium excretion, and plasma volume expansion, culminating in BP elevation.…”

Correlation Between Covid-19 Deaths and Social Indicators in Northeast Brazil

“…As also Petto [19] et al (2021) speculate that by inactivating ACE2, the virus provides greater activity of ACE1, of the Ang II receptors of the Renin Angiotensin System (RAS) that favors the evolution of diseases and consequently worsen the prognosis of infected patients, since hypertensive and diabetic patients show an increase in inflammatory markers and stimulate the disease cycle with the RAS resulting from the inflammatory process [20,21], responsible for reducing the immune reserve, thus the virus installs easily and aggressively [19,22].…”