Clinical data and experimental studies have established the important role of abnormal lipid metabolism in the causation of atherosclerosis and enthroned the hydroxymethylglutaryl coenzyme reductase inhibitors (statins) as a mainstay in management of patients with coronary heart disease. However, emerging experimental data underline the role of vascular renin-angiotensin systems in mediating the early stages of vascular endothelial dysfunction and inflammation as prerequisites for unleashing the cascade of cellular and molecular events that lead to the deposition of foam cells and their eventual progression to the atherosclerotic plaque. We discuss here the biological effects of statins and angiotensin II in the evolution of atherogenesis, underscoring possible links between statins and angiotensin receptor blockers. From the assessment of the commonality of effects resulting from the nonlipidic actions of statins and angiotensin II on the process of atherogenesis, we develop the argument that dyslipidemia may influence the ability to control blood pressure in hypertensive subjects and hypothesize that the combined use of statins and blockers of the renin-angiotensin system may have an additive effect in the management of hypertensive subjects.