Pathogenesis of the atherosclerotic process is deemed as multi-factorial, and characterized by chronic inflammatory response. Although hypertension is known to be one of the most important risk factors for atherosclerosis in causasians, its relative contribution to early atherosclerosis are still unknown. Increased evidence has indicated that hypertension, through the vasoactive peptides, such as angiotensin and endothelin-1, promotes and accelerates the atherosclerotic process via inflammatory mechanisms. In animal and human studies pro-inflammatory properties of angiotensin II has been demonstrated in large conduit and small arteries, in the kidney as well as in the heart. Activation of oxidative stress by angiotensin II is a key component of this process. Angiotensin II stimulates nicotinamide adenine dinucleotide phosphate/nicotinamide adenine dinucleotide oxidase in endothelium, smooth muscle cells, and the adventitia of blood vessel to generate reactive oxygen species, leading to endothelial dysfunction, growth, and inflammation, upregulation of endothelin-1, adhesion molecules, nuclear factor-kappa B, and other inflammatory mediators, as well as increased breakdown of nitric oxide and uncoupling of nitric oxide synthase, contribute to the progression of vascular disease and atherogenesis. In addition, recent advances concerning role of endothelin-1 as another important mediator of chronic inflammation in the vascular wall has been documented, and relationship between endothelin-1 and angiotensin II on vascular inflammation demonstrated. Inflammatory mechanisms, therefore, are important participants in the pathophysiology of hypertension-related cardiovascular disease, including atherosclerosis. In experimental models as well as human studies of atherosclerosis, angiotensin converting enzyme inhibitors or angiotensin II receptor blockers have demonstrated the ability to prevent or reverse the progression of atherosclerosis, which was in part associated with decreased expression of inflammatory mediators and improve endothelial functions. Based on those increasing evidence, we hypothesize that inflammation may be a bridge connecting hypertension and atherosclerosis.