Current national guidelines have recommended the use of renin-angiotensin system inhibitors, including angiotensin II type 1
receptor blockers (ARBs), in preference to other antihypertensive agents for treating hypertensive patients with chronic kidney disease.
However, the mechanisms underlying the renoprotective effects of ARBs are multiple and complex. Blood pressure reduction by systemic
vasodilation with an ARB contributes to its beneficial effects in treating kidney disease. Furthermore, ARB-induced renal vasodilation
results in an increase in renal blood flow, leading to improvement of renal ischemia and hypoxia. ARBs are also effective in reducing
urinary albumin excretion through a reduction in intraglomerular pressure and the protection of glomerular endothelium and/or podocyte
injuries. In addition to blocking angiotensin II-induced renal cell and tissue injuries, ARBs can decrease intrarenal angiotensin II levels
by reducing proximal tubular angiotensinogen and production of collecting duct renin, as well as angiotensin II accumulation in the kidney.
In this review, we will briefly summarize our current understanding of the pharmacological effects of an ARB in the kidney. We will
also discuss the possible mechanisms responsible for the renoprotective effects of ARBs on type 2 diabetic nephropathy.