Diabetic neuropathic pain is a common symptom of diabetic neuropathy, which is a complication that affects many people living with diabetes and is caused by damage to nerves. To date it is acknowledged that neurodegeneration of the somatosensory nervus system underlies the development of this neuropathology however the mechanisms in which this arises are not yet certain. The sensory neurons in the dorsal horn of the spinal cord are typically hyperactive in diabetic individuals and there is now evidence reporting microvessel damage as a putative cause. Pericytes are cells found along microvessel walls and have been found to constrict blood vessels in other diabetes-linked complications such as retinopathy as well as other neurodegenerative conditions (e.g. Alzheimers), reducing blood flow to vital systems. In this study, the mechanism of pericyte contractility via angiotensin II, an effector molecule upregulated during hyperglycaemia, was explored as a direct link to diabetic neuropathy. Fluo-4 calcium assays in the presence of angiotensin II as well as immunocytochemistry staining were performed on pericytes extracted from 7-day-old C57BL/6 wild type mouse spinal cords (n=6). All animal studies were reviewed by Nottingham Trent University AWERB and performed in line with ASPA legislation. Immunocytochemistry demonstrated that a large proportion of isolated spinal cord cells were neuron-glia 2 (NG2) positive, indicating isolated cells were pericytes (99.6% (****p<0.0001, Unpaired T Test comparing percentage of cells with and without NG2 expression)). In addition, angiotensin II dose dependently led to a pronounced increase in intracellular calcium immediately post application. 100nM angiotensin II led to the most prominent peak calcium response (****p<0.0001, One way ANOVA comparing peak calcium response across all angiotensin II concentrations) and greatest prolonged calcium response (**p<0.001, One way ANOVA comparing the area under the curve produced by all concentrations of angiotensin II when applied to pericytes). It can be concluded that angiotensin II produces contraction of spinal cord pericytes, which is explanatory of the increased calcium response. This suggests that this mechanism may be involved in constriction of microvessels, leading to nerve ischemia and diabetic neuropathic pain, however further research is needed to confirm this interaction and its mechanisms.