A variety of disturbances in transmembrane monovalent and divalent cation fluxes has been described in blood cells from hypertensive patients. Other membrane properties, such as fluidity and calcium binding, are also altered. It is now abundantly clear that some of the inconsistencies in this field are due to poor matching of patients and controls. However, even when careful matching is carried out, differences in membrane functions are still seen. It is suggested that these are due to a disturbance in the physicochemical properties of the cell membrane, related to changes in cell membrane phospholipid fluidity. This change could maintain peripheral resistance either by directly or indirectly increasing tone or by predisposing to resistance vessel hypertrophy. Recent evidence emphasizes the role of the latter rather than the former in experimental hypertension. It is postulated that overactivity of the phosphoinositide second messenger system as a result of alteration in all membrane properties predisposes genetically susceptible individuals to resistance-vessel hypertrophy and hypertension.