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It is known, in fact, that SARS-CoV-2 causes ACE2 downregulation impairing the ACE2-mediated Ang II conversion into Ang 1-7 with the loss of its vasodilatory, anti-inflammatory, antioxidant, and anti-atherosclerotic proprieties and of their protective impact on COVID-19 morbidity and mortality [[5]]. In vivo human data that may address the beneficial role of RAS blockers in COVID-19 and its complications may be provided by patients with Gitelman's and Bartter's syndromes (GS/BS). Keywords: Bartter's syndrome; Angiotensin II; RAS blockers; COVID-19; Gitelman's syndrome EN Bartter's syndrome Angiotensin II RAS blockers COVID-19 Gitelman's syndrome 593 596 4 11/14/22 20221220 NES 221220 The renin-angiotensin system (RAS) during COVID-19 pandemic has captured the interest as the severe coronavirus 2 (SARS-CoV-2) causing COVID-19 uses angiotensin-converting enzyme type 2 (ACE2) as an entry point into the cell [[1]]. [Extracted from the article]

Background: Gitelman's and Bartter's syndromes (GS/BS) are rare genetic tubulopathies characterized by electrolyte imbalance and activation of the renin-angiotensin-aldosterone system (RAAS). These syndromes have intriguing biochemical and hormonal abnormalities that lead them to be protected from hypertension and cardiovascular and renal remodeling. Summary: In this review, we explore the biochemical/molecular mechanisms induced by the activation of the RAAS and its counterregulatory arm which is particularly activated in GS/BS patients, in the context of blood pressure regulation. In addition, we report our findings in the context of the COVID-19 pandemic where we observed GS/BS subjects being protected from infection. Key Messages: The intracellular pathways induced by Ang II, starting from induction of oxidative stress and vasoconstriction, are crucial for the progression toward cardiovascular-renal remodeling and might be useful targets in order to reduce/halt the progression of Ang II/oxidative stress-induced cardiovascular-renal morbidity in several diseases. [ABSTRACT FROM AUTHOR]