The cardioprotective nature of oestrogen is perceivable through increased cardiovascular disease incidence rates in women post-menopause. One of oestrogen’s protective mechanisms is inducing vasodilation through non-genomic, rapid signalling to increase nitric oxide (NO) production. Genomic upregulation of this pathway is facilitated by oestrogen-responsive genes. This study proposes a novel pathway of oestrogen-induced vasodilation and the influence of ageing and oestrogen status. A scoping review examined literature on oestrogen within the vascular system to find potential interactants and the impacts of ageing and oestrogen status upon these. The results indicate 8 new proteins interact with endothelial nitric oxide synthase (eNOS), producing NO and stimulating vasodilation. Ageing and oestrogen deficiency downregulate, seen in women post-menopause, cause a decrease in overall vasodilation which decreases vascular health. Distinct ER gene polymorphisms were observed associated with cardiovascular pathological phenotypes. Increased methylation of ERα and β CpG sites were detected in atherosclerotic tissues. These results and further advancements have potential impacts through identification of pharmacological targets, prevention of cardiovascular disease using oestrogen’s cardioprotective pathways and mechanisms, epigenetic modification, and personalised medicine to reduce cardiovascular disease incidence.