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

Figures

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  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.

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  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.