The concept of hypertension as primarily a consequence of altered hemodynamics has changed. Many factors are now implicated in the development of hypertensive vascular disease, and the renin-angiotensin-aldosterone system (RAAS) appears to be one of the most significant. Angiotensin II, the principal effector peptide of the RAAS, has far-reaching effects on vascular structure, growth and fibrosis, and is a key regulator of vascular remodeling and inflammation. Reactive oxygen species and a network of signaling pathways mediate angiotensin II and cellular mechanisms that promote remodeling and inflammation. The involvement of aldosterone in vessel-wall and myocardial remodeling has also come under intensive research scrutiny. Treatments that block the pathologic effects of the RAAS at several points have been shown to limit target-organ damage in hypertension and to decrease cardiovascular morbidity and mortality. Understanding the molecular and cellular mechanisms that participate in the early development of hypertensive vascular disease may lead to more targeted treatment and improved outcomes.