The plasticity of cellular Ca2+ control and the events regulated by [Ca2+]i and other messengers make it difficult to assign causative or consequential roles to deranged platelet Ca2+-linked processes in the pathophysiology of essential hypertension. Our studies in human platelets support an underlying membrane pathology as being causative since observed derangements including partial membrane depolarization and enhanced calcium influx, enhanced hormone responsiveness and coupling to adenylate cyclase, increased phosphoinositide metabolism, as well as stimulated Ca2+-ATPase extrusion activity are membrane associated systems. Modification of phosphoinositide metabolism may be a key factor accounting for the multifaceted membrane abnormalities and eventually contribute to the elevated cytosolic [Ca2+]i concentration in essential hypertension. Whether these membrane abnormalities can also be found in human smooth muscle cells has yet to be determined.