A lthough the causes of high blood pressure vary, it / \ is becoming clear that sustained hypertension is -Z A . associated with changes in cardiovascular structure: left ventricular hypertrophy and increased wall thickness:lumen diameter (wall:lumen) ratio of the blood vessels. To some extent, these alterations are natural physiological responses and are protective. However, the risk of circulatory death is closely related to left ventricular hypertrophy, and therefore, it is suggested increasingly that effective antihypertensive treatment requires normalization not only of blood pressure but also of cardiac structure. This may be the case also for the vascular changes, in particular at the level of the "resistance arteries" (defined here as precapillary arteries with diameters less than 500 fim; see Reference 2), these vessels being responsible for the increased peripheral resistance of essential hypertensive patients. Until recently, this possibility remained speculative because there were few quantitative data concerning resistance artery structure. However, over the past 10 years such data have become available, in particular with regard to the more proximal resistance vessels, so-called "small arteries" (see Reference 2). The purpose of this Brief Review is to identify the type of structural change that is found in small arteries in hypertensive individuals. In particular, we will discuss whether the altered structure can be ascribed to growth alone or whether it is due to "remodeling,"' that is, a rearrangement of otherwise normal material, which Baumbach and Heistad first noted in cerebral small arteries of spontaneously hypertensive rats (SHR) that are stroke-prone.