1. Increased affinity for
sodium (Km) at an external site of the
sodium-lithium countertransporter and altered membrane microviscosity in the surface regions of the
lipid bilayer identifies a group of essential hypertensive patients with a
genetic predisposition to
hypertension. The present study investigated the kinetic properties of the
sodium-lithium countertransporter and membrane microviscosity in patients with
hypertension, renal disease and impaired renal function. 2. Sixty patients with renal disease (28
chronic renal failure, 30 hypertensive, 23 family history of
hypertension) were investigated. Standard erythrocyte
sodium-
lithium countertransport activity,
sodium affinity constant (Km), maximum reaction velocity (Vmax) and membrane microviscosity were measured. 3. Patients with renal disease and a family history of
hypertension had significantly lower Km (P < 0.05) values and raised membrane microviscosity measured by 1-(4-trimethylammoniumphenyl)-6-phenyl-1,3,5-hexatriene anisotropy (P < 0.05) compared with patients without a family history of
hypertension. 4. Uraemic subjects had low K(m) values compared with patients with renal disease and normal renal function (P < 0.05). However, there was no significant difference in membrane microviscosity between uraemic and non-uraemic subjects. 5. In patients with a family history of
hypertension,
sodium-
lithium countertransport activity and 1-(4-trimethylammoniumphenyl)-6-phenyl-1,3,5-hexatriene anisotropy are important markers of cellular changes in
essential hypertension, independent of renal disease. Uraemia, independently of
hypertension, produces an alteration in the function of the
sodium-lithium countertransporter which has previously been associated with a
genetic predisposition to
hypertension and
cardiovascular disease.