SARS-CoV-2 e hipertensão : evidências suportam a invasão do cérebro por meio da circuitaria do barorreflexo e o papel do desbalanço do sistema renina-angiotensina-aldosterona

Abstract

A precise understanding of COVID-19 and its prognosis requires a broad and integrative look at the relationship of SARS-CoV-2 with different structures and tissues. The endothelium and the CNS have been shown to be key players in this process. Endothelial infection by SARS-CoV-2 can result in vascular weakening, which has been associated with the entry of the virus into multiple organs and structures, especially large vessels and the brain. The present study is a literature review that aimed to: 1) describe a new possible neuroinvasion route of SARS-CoV-2, from baroreceptors; and 2) investigate the possible relationship between ANG-II and ADAM17, associated with SARS-CoV-2 infection, and neurogenic hypertension. SARS-CoV-2 infection in human cells favors an imbalance of the RAAS, characterized by increased activity of its pro inflammatory and pro-hypertensive axis (ANG II/AT1R), and ADAM17/TACE. Evidence indicates that the virus's access to baroreceptors, present in large vessels, may allow the virus to enter the brain. Therefore, direct and indirect effects of the virus on the CNS can significantly impact blood pressure control. The reduction in the integration of inputs that reach the NTS from the baroreceptors, in addition to the activation of the PVN, are mechanisms related to the increase in sympathetic activity, which can be triggered by the invasion of SARS-CoV-2. In a pioneering way, we proposed a possible central mechanism capable of explaining the emergence or worsening of systemic hypertension, and the development of a worse prognosis of COVID-19. The relationship between COVID-19 and the development or worsening of hypertension has been demonstrated in recent publications. However, more studies are needed in order to experimentally verify the hypotheses defended here.