Vinothkumar Ganesan

By Vinothkumar Ganesan

Renin angiotensin aldosterone (RAAS) is very well established as a regulator of blood pressure (BP) and a determinant of target organ injury. It controls fluid and electrolyte balance through coordinated effects on the heart, blood vessels, and kidneys. The main effector of RAAS is angiotensin II (Ang II), which exerts its vasoconstrictor effect primarily on the postglomerular arterioles, thereby raising the glomerular hydraulic pressure and ultrafiltration of plasma proteins, which may lead to the initiation and progression of chronic kidney disease (CKD). RAAS also plays a, key role in hypertension and cerebrovascular disease. Enhanced Ang II levels accelerate the initiation and progression of cell senescence by fostering inflammation and oxidative stress. Sustained activation of RAAS facilitates aging-related CKD and results in cognitive dysfunction and Alzheimer’s disease (AD). However, in many hypertension treatment studies, the frequency of fatal and nonfatal stroke has been greatly reduced, and this is very important since a history of stroke doubles the risk of dementia in both patients without CKD and hemodialysis. In CKD patients with AD, anemia has also been identified as a risk factor for cognitive impairment, and correction of anemia with recombinant erythropoietin treatment has been shown to enhance cognition measures, such as AD markers and neuropsychological tests.

Part of the book: Renin-Angiotensin Aldosterone System