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    • Use of RASB is associated with potential

    2023-01-28

    Use of RASB is associated with potential concerns about side effects such as acute kidney injury or hyperkalemia, and clinicians are reluctant to prescribe RASB in patients with severe renal dysfunction (estimated GFR <30mL/min/1.73m2). In addition, although CKD is common in patients with HF, there is a lack of evidence-based therapies in patients with severe renal dysfunction because most randomized controlled trials have excluded these patients. However, some registry data show that treatment with RAS blockade was associated with improved survival in patients with severe renal dysfunction [26], [27]. In accordance with previous studies, better survival associated with ARB use compared with no use of RASB was observed in patients with severe renal dysfunction. Randomized controlled trials are needed in order to apply these findings to clinical practice. Use of RASB in addition to a beta-blocker is recommended for symptomatic patients with HFrEF to reduce the risk of HF hospitalization and death [11]. In accordance with the current guideline, our data showed that the effects of ARB were greater in patients without prescription of beta-blockers at discharge than in those with prescription of beta-blockers at discharge. RASB should be considered for reduction of mortality and morbidity in patients with HFrEF who have a contraindication of beta-blockers.
    Conclusions
    Conflict of interest
    Acknowledgement
    Introduction Renin-angiotensin system (RAS) was initially described as a hormonal circuit controlling body electrolyte balance and blood pressure (Campbell, 1987; Ribeiro et al., 1985). Angiotensinogen produced by liver is cleaved by kidney-synthesized renin to a decapeptide angiotensin I, which is further processed by endothelial angiotensin-converting enzyme (ACE) to angiotensin II (Ang II). Predominant target of Ang II in adult tissues is type 1 receptor (AT1), expressed by many cell types, including endothelial and smooth muscle cells. AT1 is a seven-domain transmembrane receptor, which initiates many intracellular signaling cascades including Ca mobilization. As a net result Ang II causes blood vessel wall contraction and increases the blood pressure (Dinh et al., 2001). Ang II also causes inflammation and fibrosis in AT1-dependent manner (Brasier et al., 2002; Linz et al., 1995; Mezzano et al., 2001). Besides AT1, Senexin B could also express type 2 angiotensin receptor (AT2). Ang II binding to AT2 is thought to counterbalance negative effects triggered by AT1, since it causes anti-inflammatory, anti-fibrotic response (Dinh et al., 2001; Horiuchi et al., 2012). Despite in embryogenesis both AT1 and AT2 are highly expressed, the presence of AT2 declines soon after birth (Lazard et al., 1994; Shanmugam and Sandberg, 1996). As a beneficial system, counteracting detrimental effects of Ang II/AT1 axis, “alternative angiotensin peptides” could be produced, including angiotensin 1–7 and alamandine, which interact to MAS1 and MrgD receptors (reviewed in Carey, 2013; Etelvino et al., 2014). Together with circulating RAS, a local production of angiotensinogen and its processing enzymes was found in several organs, including kidney, brain, heart, pancreas and adipose tissue (Campbell, 1987; Cassis et al., 2008; Danser, 1996). Ang II production by adipocytes increases during pathologies associated with obesity (Engeli et al., 2000; Henriksen et al., 2001). Its significance for adipose tissue growth and metabolism is intensively studied. The main precursors for adipocytes are mesenchymal stem cells of adipose tissue (ADSCs) (Hausman et al., 2001; Pittenger, 1999; Scavo et al., 2004), and adipose tissue hyperplasia seems to depend on the adipogenic potency of ADSCs and their further differentiation to adipocytes.
    Material and methods
    Results
    Discussion Despite renin-angiotensin-aldosterone system has been studied for a long time, its role in various physiological and pathological processes still attracts close attention, first of all because pharmacological instruments for influencing RAS activity in humans are accumulated. In this study we demonstrated the expression of angiotensin receptors in stromal compartment of human adipose tissue in situ. Specifically, our data indicate that ADSCs of adipose tissue stroma demonstrate a heterogeneous expression of angiotensin receptors and produce angiotensinogen together with enzymes necessary for angiotensin peptides generation. These data advance previous observations that angiotensinogen is one of adipokines produced by pre-adipocytes and mature adipocytes, which expression increases with lipids accumulation (Safonova et al., 1997). Also, these data confirm previous findings obtained in ADSC lines (Chen et al., 2012; Matsushita et al., 2006) and indicate that local RAS is important for the regulation of ADSCs functioning within adipose tissue.