The consequence of a sustained rise in blood pressure is an adaptive change in the structure of the heart and the vasculature. In humans, the left ventricle, aorta, and medium-sized arteries undergo hypertrophy whereas the changes in resistance vessels are unclear at present. Recent studies suggest that left ventricular hypertrophy is a better predictor of stroke or cardiac risk than age or blood pressure. Therefore, the cellular mechanisms that bring about these structural alterations to the circulation in hypertension are the subject of intense research at this time. The main factor was assumed to be the pressure load imposed on the wall of the left ventricle and the arteries. However, recent work has suggested that pressor hormones can act as growth factors in vascular tissues by pressure-independent actions. This article examines the cellular mechanisms activated by angiotensin II that could be involved in producing growth and the evidence available that this nonpressor role is important in vitro and in vivo.