A wide range of abnormalities of membrane sodium and potassium transport can be demonstrated in patients with essential hypertension, and in rats with genetic hypertension and with some forms of experimental hypertension. In the human red cell increased permeability to sodium and potassium, increased ouabain-sensitive sodium pumping, lithium-sodium counter-transport, and frusemide-sensitive co-transport have been described; by contrast, in the human leucocyte sodium pumping is reduced. In the spontaneously hypertensive rat and the rat with mineralocorticoid-induced hypertension, increased permeability to sodium and potassium, with increased ouabain-sensitive pumping, is shared by the red cell and the arterial smooth muscle. This abnormality is associated with decreased cell-membrane affinity for calcium and increased cell-membrane viscosity. It is proposed that in essential hypertension the decreased membrane affinity for calcium is a primary pathogenetic change giving rise to secondary changes in sodium and potassium transport.