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  • To the best of our knowledge this

    2022-11-18

    To the best of our knowledge, this is the first study documenting the SCC modulatory effect at central and kidney level on the shift in the vasoconstrictor-vasodilator ratio of mRNA expression of angiotensin receptors toward vasoconstriction in XY-SCC and/or vasodilation in XX-SCC mice. From these results and those of other authors we can thus infer that both the activational hormonal effects (Baiardi et al., 2005, Miller et al., 1999, Silbiger and Neugarten, 1995) and the SCC factors are involved in sexually dimorphic mRNA expression of angiotensin receptors. This may constitute the basis of a shift in the functional sexually dimorphic angiotensin responses and in the incidence of cardiovascular diseases among males and females.
    Sources of funding This study was supported in part by grants from Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET) [N°2561], Agencia Nacional de Promoción Científica y Tecnológica (ANPCyT) [N° 1580]. International Society for Neurochemistry (ISN) [year 2015], Ministerio de Ciencia y Tecnología de la Provincia de Córdoba (MinCcyt) [N°113/2011] and Secretaria de Ciencia y Tecnología (SECyT-Universidad Nacional de Córdoba) [N°1565]. FAPESP [#2013/0799-1] and CNPq [N°301827/2011-7 and 401598/2014-4] to JAR; MJC, AG, LV and XEC are members of CONICET. FMD, CDC and AFM hold fellowships for CONICET.
    Acknowledgments
    Introduction The renin angiotensin (Ang) system (RAS) consists of angiotensinogen from liver gets converted to Ang I by renin, a protease mainly produced from the juxta-glomerular 2768 of the kidney. Ang I converting enzyme (ACE), a dipeptidyl carboxypeptidase mainly produced by the lungs, hydrolyzes Ang I to Ang II. Many of the physiological as well as pathological roles of RAS are mediated mostly via Ang II acting on its receptors of two categories; Ang II type 1 receptor (AT1R) and type 2 receptor (AT2R) both belonging to a family of G-protein coupled receptors (Fig. 1). This is central to the pathogenesis of cardiovascular (CV) disease through increase in reactive oxygen species (ROS) and oxidative stress, causing vascular inflammation and remodeling, endothelial dysfunction, and atherosclerosis with subsequent complications such as myocardial infarction (MI), stroke, chronic heart failure (HF), and renal disease [1]. Contemporary RAS inhibition includes use of ACE inhibitor (ACEI) and/or AT1R blocker (ARB), which has become a leading therapeutic strategy in slowing the progression of HF and kidney diseases. ARBs have gained prominence in therapy of many pathological conditions; one possible advantage is that by blocking AT1R, ARBs enhance Ang II activity on AT2R. It may also influence the conversion of Ang II to other mediators of RAS such as Ang (1–7) by ACE2 that acts on Mas receptor (Fig. 1). This newer axis composed of ACE2/Ang (1–7)/Mas is suggested to produce some beneficial actions against the pathological role of Ang II. As new components and functions of RAS are being unraveled, focus is now shifting from the classical effects of RAS effectors such as regulation of intravascular volume and systemic blood pressure (BP) to their non-classical actions. Endogenous Ang II could be a key element in the immunomodulation of T-cell responses, such as activation and posterior adhesion/ transmigration activity [2]. The elucidation of such mechanisms could help to understand the Ang II-induced inflammation process and to improve treatment outcomes of immune-based diseases. We have also identified and reported the role of various ARBs against HF induced by experimental autoimmune myocarditis in rats [3], [4]. Recent reports also suggest the importance of RAS blockade during diabetic complications such as cardiomyopathy, nephropathy, and neuropathy. This review focuses on the recent advances in individual ARBs (Fig. 2) as therapeutic agents against various cardiac and renal pathologies (Fig. 3). The order of the ARBs presented here is based on their popularity and not considering their efficacy or other parameters.