Figure 2.

Role of EVs in the development and progression of hypertension. Risk factors for hypertension-induced events cause the release of systemic and urinary EVs from various cells. EV activation contributes to the pathogenesis of hypertension and hypertension-induced events, such as vascular and kidney dysfunction, including impaired endothelial function, VSMC proliferation and migration, altered NHE3, NCC, ENaC activity, and maladaptive of RAS. These processes collectively contribute to the development and progression of hypertension. EVs: extracellular vesicles; VSMCs: vascular smooth muscle cells; NHE3: sodium/hydrogen exchanger type 3; NCC: sodium chloride cotransporter; ENaC: epithelial sodium channel; RAS: renin-angiotensin-system.