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The balance of angiotensin II and nitric oxide determines the sensitivity of the tubuloglomerular feedback mechanism, renal vascular resistance and filtration rate. Angiotensin II induces nitric oxide release, but the role of angiotensin II receptors here is not fully understood. Further, the angiotensin II–nitric oxide interaction can be modulated by reactive oxygen species. This review focuses on the angiotensin II–nitric oxide interaction and their modulation by reactive oxygen species in the control of renal blood flow.Ideas about the role of angiotensin II type 1 and angiotensin II type 2 receptors are extended by the observation of angiotensin II type 1-mediated nitric oxide release with direct effects on vascular tone, tubuloglomerular feedback and sympathetic neurotransmission. Angiotensin receptors elicit disparate effects on intrarenal circulation. Angiotensin II–nitric oxide interactions are modulated by reactive oxygen species, as shown by angiotensin II type 1-mediated activation of superoxide and depression of antioxidant enzymes leading to reduced nitric oxide concentration – mechanisms that may be also important in angiotensin II-dependent hypertension.Recent studies show that angiotensin II stimulates the nitric oxide system via angiotensin II type 1 and angiotensin II type 2 receptors, whereas receptors exert different effects on renal and medullary flow. The interaction via angiotensin II type 1 is modulated by reactive oxygen species.