REDUCED NITRIC OXIDE BIOAVAILABILITY AS A FACTOR OF ENDOTHELIAL DYSFUNCTION IN RENAL ARTERIOLES UNDER HYPERURICEMIA

This work examines the role of reduced nitric oxide (NO) bioavailability as a key factor in the development of endothelial dysfunction of renal arterioles under hyperuricemic conditions. Elevated serum uric acid promotes oxidative stress, inflammation, and inhibition of endothelial nitric oxide synthase, leading to NO inactivation. The resulting endothelial dysfunction causes persistent vasoconstriction, impaired microcirculation, and increased intraglomerular pressure, contributing to renal ischemia, interstitial fibrosis, and progression of chronic kidney disease. Understanding these molecular mechanisms is crucial for developing targeted therapeutic strategies to prevent vascular and renal complications associated with hyperuricemia.