Type 2 Diabetes Mellitus (T2DM) and hypertension (HTN) both increase cardiovascular disease (CVD) morbidity and mortality, and impose a tremendous burden on worldwide heath care systems in recent years. The mechanisms underlying the frequent coexistence of T2DM and HTN, two main components of the Cardiometabolic Syndrome (CMS), remain to be fully uncovered. Interestingly, both conditions are linked by chronic inflammatory processes and insulin resistance that are instigated by enhanced activation of the Renin Angiotensin Aldosterone System (RAAS). Inappropriate activation of the RAAS and insulin resistance with compensatory hyperinsulinemia trigger numerous pathophysiological pathways that ultimately result in endothelial dysfunction, inflammation, proliferation, and remodeling in cardiovascular and renal tissue. Blockade of RAAS has proven beneficial in the management of T2DM and HTN as well as associated CVD and chronic kidney diseases. This review focuses on current knowledge about the role of RAAS and insulin resistance and accompanying inflammation and oxidative stress in the pathophysiology that links DM and HTN.