Mechanistically, the blood pressure-lowering effects of ARBs are well-established through blockade of the angiotensin II type 1 receptor, leading to vasodilation and reduced aldosterone secretion. The PARASOL study's findings align with this pathway, where sacubitril/valsartan's combined neprilysin inhibition and AT1 receptor blockade showed efficacy in hypertensive Japanese adults (Yamamoto 2024). Preclinical and mechanistic data suggest that ARBs may influence metabolic pathways, as indicated by the significant HbA1c and glucose reductions with sacubitril/valsartan treatment (Abhari 2026). Furthermore, the observed renal hemodynamic effects, such as changes in intrarenal blood flow, may contribute to the variable outcomes seen in CKD populations (Wever 2025).

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