We have reviewed studies of the role played by abnormalities of vascular smooth muscle in hypertension. The basic contractile apparatus of this muscle appears to be qualitatively normal, but the synthetic function of the cell is exaggerated so that more contractile protein is produced. Activation pathways of the smooth muscle cell, initiated by phospholipase C, are enhanced. A reduced ability of the endothelium to produce vascular smooth muscle relaxation may contribute to an enhanced contraction of this muscle in hypertension. Furthermore, the intrinsic cellular mechanisms that produce relaxation of this muscle may also be impaired in hypertension. However, the many abnormalities observed in membrane transport systems in this muscle in hypertension suggest that the primary defect in the cell may be a lack of stability in the membrane caused by an impairment in its ability to bind calcium.