Cerebral arterioles in stroke-prone spontaneously hypertensive rats (SHRSP) undergo remodeling with a reduction in external diameter, paradoxically becoming more distensible, despite hypertrophy of the vessel wall. Two concepts have been proposed. (1) Remodeling of cerebral arterioles is an important mechanism, in addition to hypertrophy, of encroachment on the vascular lumen in SHRSP. (2) Increases in arteriolar distensibility partly compensate cerebral arterioles for other factors, such as hypertrophy and remodeling, which reduce the dilator capacity of these arterioles in chronic hypertension. Recently, we have studied the effects of reducing blood pressure by drug treatment or carotid clipping on hypertrophy and remodeling of cerebral arterioles in SHRSP. Our findings suggest that (1) pulse pressure may be a more important stimulus than mean pressure for hypertrophy of cerebral blood vessels and (2) remodeling of cerebral arterioles may occur independently of hypertrophy. Treatment that effectively prevents vascular hypertrophy during chronic hypertension may not be effective in preventing remodeling, and may therefore fail to restore cerebral vascular function to normal.