Activation of the renin-angiotensin system (RAS) and aberrant cholesterol metabolism have generally been considered as independent mechanisms in the development of several vascular diseases. However, it is becoming increasingly apparent in both human and animal studies that many aspects of the RAS may be augmented by hypercholesterolemia, resulting in enhancement of the severity and occurrence of several vascular diseases, including hypertension, atherosclerosis and abdominal aortic aneurysms. Some potential hypercholesterolemia-induced mechanisms have been demonstrated to increase activity of specific components of the RAS. These include increased AT1-receptor expression, increased responsiveness to Ang II and increased synthesis of angiotensin peptides. Future studies need to validate mechanisms of hypercholesterolemia-induced RAS activation in different vascular diseases.