The purpose of the work described in this thesis was twofold. Firstly, to determine what role nitric oxide (NO) played in renal warm ischaemia reperfusion injury and secondly, once the role was clarified, to assess if this injury could be ameliorated by the pharmacological manipulation of renal NO. The introduction to this thesis comprises two parts. Chapter 1 reviews the pathophysiology of renal ischaemia reperfusion and outlines some of the treatment modalities that have been used in response. Chapter 2 focuses on the physiology of NO and the pathophysiological role it plays in renal reperfusion injury and contrasts some apparent differences between the kidneys and other organs. The three main experimental Chapters are then presented. The first of these describes the development and verification of a NO assay for use with renal tissue homogenate. The next Chapter describes the development of a new model of renal warm ischaemia reperfusion injury in a rodent model which allows the collation of renal NO levels with comparative renal functional, pathological and pathophysiological data. The final experimental Chapter details both the effect of warm ischaemia reperfusion injury on renal NO generation and the subsequent effect of pharmacologically manipulating NO on the degree of renal injury sustained. In the final Chapter the experimental results are reviewed and possible avenues of further investigation are discussed.