Table 1.

Interactive mechanisms underlying hypertension and kidney injury in atherosclerotic RASa

Tissue UnderperfusionRecurrent Local Ischemia
Activation of renin-angiotensin systemATP depletion
Altered endothelial function (endothelin, NO, prostaglandins)Tubulointerstitial injury
Sympathoadrenergic activationMicrovascular damage
Increased reactive oxygen speciesImmune activation
Cytokine release/inflammation (NF-κB, TNF, TGF-β, PAI-1, IL-1)Vascular remodeling
Impaired tubular transport functionsInterstitial fibrosis
Apoptosis/necrosisRAAS
Sympathoadrenergic activation
Endothelin
Disturbances of “oxidative stress”
Oxidized LDL
  • a NO, nitric oxide; PAI-1, plasminogen activator inhibitor-1.