The presence of diabetes (70%–75% of models) contributes to HTN through insulin resistance, formation of advanced glycation end products, endothelial dysfunction, oxidative stress, deregulation of the renin-angiotensin-aldosterone system, and sodium retention, with a 1.5–2.5 times higher risk of presenting HTN compared to non-diabetic individuals (40). This evidence concerns the gene REN and endothelial dysfunction.