This paper reviews the evidence that the resistance vasculature is altered in hypertension and the role that the vasculature may play in the pathogenesis of the disease. Although functional changes (i.e., increased vascular smooth muscle sensitivity) have been found to be associated with some models of hypertension (e.g., spontaneously hypertensive rat), in human essential hypertension it appears that the abnormalities that predominate in the resistance vasculature are structural in nature. These changes result in an increased media/lumen ratio of the more proximal resistance vessels (i.d. 100-300 microns), and the changes are such that they could account for many of the altered hemodynamic characteristics seen in patients with essential hypertension (e.g., increased minimum vascular resistance, increased pressor response). However, evidence that the abnormal structure of the peripheral vasculature is a prime determinant of blood pressure is still lacking, and much of the available evidence suggests that the altered structure is a secondary adaptation. Nevertheless, the abnormal vascular structure may play an important pathological role concerning the morbid consequences of the hypertensive disease, suggesting that normalization of vascular structure is a desirable aim for antihypertensive treatment. At present it seems that treatment must be continued for long periods, maybe many years, before vascular structure is normalized.