Renal renin–angiotensin system (RRAS)

The renal renin–angiotensin system refers to the local (intrarenal) expression and activity of the broader renin–angiotensin(-aldosterone) system within kidney tissues. Its components—renin, angiotensinogen, angiotensin-converting enzyme (ACE), angiotensin peptides, and angiotensin receptors (primarily type 1, AT1)—are produced and act locally in the nephron and renal vasculature. This system tightly regulates kidney hemodynamics, glomerular filtration, sodium reabsorption, water balance, as well as contributing to pathophysiological processes such as hypertension, fibrosis, and kidney damage. It can function independently of the circulating endocrine RAS and is an important focus for understanding and treating cardiorenal diseases.

Other names

intrarenal renin–angiotensin systemintrarenal RASrenal RAASkidney RAS

Inhibition of renin activity (reduces Ang I and Ang II synthesis); Inhibition of ACE (prevents conversion of Ang I to bioactive Ang II); Blockade of angiotensin II receptor type 1 (blocks effects of Ang II on vasoconstriction, sodium reabsorption, aldosterone secretion, and proliferation); Antagonism of mineralocorticoid receptor (blocks aldosterone-mediated sodium retention and tissue remodeling); Inhibition of aldosterone synthesis.