Endothelial progenitor cells (EPCs) are bone marrow derived cells that contribute towards neovascularisation. I have primarily used real time polymerase chain reaction (PCR), but also flow cytometry and cell culture techniques, to investigate the effect of vascular injury on the expression of the putative markers of EPCs (CD34, CD133, VEGFR-2 and VE-cadherin) and their number in peripheral blood. In the first study I investigated the effect of percutaneous coronary intervention (PCI) on EPCs in a group of patients with stable coronary disease. After PCI, EPC markers did not conclusively demonstrate a rise in expression, although the number of VEGFR-2+ cells did increase. However, the number of EPC colony forming units (CFUs) increased significantly. In the next study, I investigated the effect of open aortic aneurysm repair on EPCs in a group of elective surgical patients. There were changes in the level of expression of EPC markers, using both real-time PCR and flow cytometry, but statistical significance was not reached. However, there were significant increases in the mean fluorescent intensities (MFI) of VEGFR-2 and VE-cadherin expression. EPC-CFUs did not change significantly. The next study investigated the effect of type 1 diabetes on EPC levels. The percentage of CD34+ cells, the RQ of VE-cadherin mRNA and the number of EPC-CFUs were significantly reduced in the diabetic cohort compared with control groups. Finally, the effect of chronic renal impairment and administration of human recombinant erythropoietin (Epo) on EPC levels was investigated. The RQs of CD34, VEGFR-2 and VE-cadherin mRNA species increased over the period analysed, but this increase did not correspond with an increase in VEGF expression. This thesis provides further insight into the effect of endogenous and exogenous causes of vascular injury on EPCs.