Renal ischaemia–reperfusion injury (IRI) increases angiotensin II (Ang II) and reactive oxygen species (ROS) that are potent modulators of vascular function. However, the roles of individual ROS and their interaction with Ang II are not clear. Here we tested the hypothesis that IRI modulates renal afferent arteriolar responses to Ang II via increasing superoxide (lass="math-equation-construct">lass="math-equation-image">l="true" class="math-equation-mathml" style="display:none">l:math xmlns:mml="http://www.w3.org/1998/Math/MathML">lns:w="http://www.wiley.com/namespaces/wiley" xmlns:wiley="http://www.wiley.com/namespaces/wiley/wiley" xmlns:cr="urn://wiley-online-library/content/render" xmlns="http://www.w3.org/1998/Math/MathML">l">Ow>2w>−l:math>) or hydrogen peroxide (H2O2).