Several disturbances of cellular Ca2+ metabolism have been described in essential hypertension and in the spontaneously hypertensive rat. Possibly the elevation of intracellular free Ca2+ concentration in arterial smooth muscle cells is one important step in the pathogenesis of primary hypertension. In most studies a decreased energy-dependent Ca2+ transport has been proposed as a mechanism. However, disturbances in cellular Ca2+ metabolism, which can be exclusively ascribed to essential hypertension, have not yet been found. The cause of altered cellular Ca2+ transport in primary hypertension may either be a genetically determined defect of membrane transport or a still-unidentified humoral factor.