The microvasculature of the neurovascular network acts as a protective barrier preventing toxic and foreign agents accessing the nervous system and supplying the integral nutrients for the nervous system to function and survive. Diabetic neuropathic pain has previously been associated with reduced perfusion of the spinal cord (1). Reduced microcirculation can be implemented in part by vasoconstrictive processes. Angiotensin II receptor type 1 (AT1) facilitates vasoconstriction and is present on several cell types including pericytes. Pericytes have been identified to cause vessel constriction (2) and highlighted within the vasculature of diabetic patients (3). Angiotensin II (AngII), a vasoactive molecule, acts through AT1 and has been observed to be elevated within neuropathic diabetic patients (4) and associated with development of pain (5). We hypothesis that reduction of microvessel diameter within the spinal cord could be a result of pericyte facilitated constriction, activated by acute effects of AngII on its receptors. The microvessels of spinal cords were investigated within adult male C57BL/6J mice (30g). Anaesthetised (using ~2% isoflurane), animals were administrated with AngII (100nm i.t., N=3) or phosphate saline buffer (age matched control+vehicle, N=3) for 10 minutes. Animals were cardiac perfused with 4% paraformaldehyde. Spinals cords were removed via laminectomy and cryoprotected (30% sucrose) overnight (4oC). 50µm tissue sections were cut for further analysis. Immunofluorescent confocal imaging of tissue sections were performed after DAPI (nucleus staining), PECAM-1 (endothelial cell) and NG2 (pericyte) labelling (Hulse et al., 2018). Fiji analysis of vessels were performed, followed by Multiple and unpaired t-test statistical analysis via GraphPad Prism with values including mean ± S.E.M. Microvessels identified in spinal cord were overall reduced (NS) in vasculature volume (4.78 ±0.22 vs. 6.83 ±1.03 P<0.1 Unpaired T-test N=3) and number (12.74 ±3.53 vs. 24.64 ±5.41 P<0.2 Unpaired T-test N=3) following AngII treatment compared to vehicle controls. Subsequently, microvessel diameter in relation to pericyte proximity was determined. PECAM-1 positive vessel diameters were recorded in reference to pericyte soma body represented by NG2 and DAPI labelling. Analysis demonstrated a reduction (NS) in mean vessel diameter in AngII vs. vehicle group (soma body 6.76 vs. 7.70 P<0.129 Multiple T-test N=3). Although results demonstrated no statistical significance, there is an overall reduction in diameter of vessels in relation to the localisation of pericyte cell bodies within the dorsal horn of spinal cords within AngII treated group vs. vehicle group. This may be supported by reduced vasculature volume and number resulting from vasoconstriction. Further use of experimental repeats would be used in future to determine significance.