The role of nitric oxide in renovascular hypertension : from the pathophysiology to the treatment.

Abstract

Renovascular hypertension is one of the most relevant causes of secondary hypertension, mostly caused by atherosclerotic renovascular stenosis or fbromuscular dysplasia. The increase in angiotensin II production, oxidative stress, and formation of peroxynitrite promotes the decrease in nitric oxide (NO) availability and the development of hypertension, renal and endothelial dysfunction, and cardiac and vascular remodeling. The NO produced by nitric oxide synthases (NOS) acts as a vasodilator; however, endothelial NOS uncoupling (eNOS) also contributes to NO reduced availability in renovascular hypertension. NO donors and NO-derived metabolites have been investigated in experimental renovascular hypertension

and have shown promissory efects in attenuating blood pressure and organ damage in this condition. Therefore, understand- ing the role of decreased NO in the pathophysiology of renovascular hypertension promotes the study and development of

NO donors and molecules that can be converted into NO (such as nitrate and nitrite), contributing for the treatment of this condition in the future.