Numerous studies performed in the past decade have shown that increased pulse pressure, an indicator of arterial stiffening, is associated with adverse clinical outcomes. Research is now focused on better defining the anatomic and physiologic determinants of increased pulse pressure. Early work considered aortic stiffening to be a passive, irreversible consequence of aging that was accelerated by hypertension. Recent studies suggest that aortic stiffening is dynamic and reversible and that abnormalities in aortic function may play a primary role in the pathogenesis of hypertension. This review summarizes current work on the genesis of increased pulse pressure and abnormal pulsatile load in hypertension, and underscores areas for future research.