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Review
. 2022 Jan 24:2022:3239057.
doi: 10.1155/2022/3239057. eCollection 2022.

Role and Mechanism of the Renin-Angiotensin-Aldosterone System in the Onset and Development of Cardiorenal Syndrome

Kexin Ma  1 , Weifang Gao  2 , Huazhou Xu  2 , Wenjie Liang  2 , Guoping Ma  1
Affiliations
Review

Role and Mechanism of the Renin-Angiotensin-Aldosterone System in the Onset and Development of Cardiorenal Syndrome

Kexin Ma et al. J Renin Angiotensin Aldosterone Syst. .

Abstract

Cardiorenal syndrome (CRS), a clinical syndrome involving multiple pathological mechanisms, exhibits high morbidity and mortality. According to the primary activity of the disease, CRS can be divided into cardiorenal syndrome (type I and type II), renal heart syndrome (type III and type IV), and secondary heart and kidney disease (type V). The renin-angiotensin-aldosterone system (RAAS) is an important humoral regulatory system of the body that exists widely in various tissues and organs. As a compensatory mechanism, the RAAS is typically activated to participate in the regulation of target organ function. RAAS activation plays a key role in the pathogenesis of CRS. The RAAS induces the onset and development of CRS by mediating oxidative stress, uremic toxin overload, and asymmetric dimethylarginine production. Research on the mechanism of RAAS-induced CRS can provide multiple intervention methods that are of great significance for reducing end-stage organ damage and further improving the quality of life of patients with CRS.

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Conflict of interest statement

There is no conflict of interest in the article.

Figures

Figure 1
Figure 1
Schematic representation of RAAS activation and its role. RAAS comprises enzymes and peptides. ① Renin secretion is increased under the condition of decreased circulating blood volume. ② Ang I promotes the secretion of norepinephrine and adrenaline, which enhance myocardial contractility and further increase cardiac output. ③ Ang II has a strong vasoconstrictive effect that acts in combination with increased cardiac output to maintain blood pressure stability. ③-④ Both Ang II and Ang III stimulate aldosterone secretion, thereby increasing circulating blood volume.
Figure 2
Figure 2
Schematic representation of RAAS-mediated CRS. ① RAAS-mediated oxidative stress not only increases the preload and afterload of the heart by inducing renal fibrosis and atherosclerosis, respectively, but also induces cardiac fibrosis, which further leads to cardiac dysfunction, reduced circulating blood volume, and ultimately renal insufficiency. ② FGF-23 alters the functional activities of the heart by inducing atrial fibrillation, left ventricular hypertrophy, and cardiac fibrosis. PBUT not only causes endothelial dysfunction but also induces cardiac dysfunction by inducing cardiomyocyte fibrosis and apoptosis. ③ RAAS-mediated ADMA production induces endothelial dysfunction by reducing NO production. Endothelial dysfunction increases cardiac preload by reducing the glomerular filtration rate, further leading to cardiac dysfunction.
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