Luft F C
Department of Medicine, Indiana University School of Medicine, Indianapolis 46223.
J Lab Clin Med. 1989 Sep;114(3):215-21.
Dietary sodium intake has long been considered important in the genesis and maintenance of hypertension. This view is predicated on the results of epidemiologic observations, experiments in animals, investigations at the cellular level, and the results from dietary intervention trials. In the past decade a considerable body of new evidence has been gathered. A comprehensive, world-wide epidemiologic investigation involving over 10,000 subjects found significant relationships between sodium excretion and blood pressure levels and between sodium excretion and the slope of increase in blood pressure with age. The relationships, however, are not as straight-forward as previously proposed. Investigations in animals and in human subjects emphasize the genetic nature of salt sensitivity of blood pressure. A putative genetic marker has been suggested in human studies. At the cellular level, increases in sodium-lithium countertransport, sodium-hydrogen exchange, and cytosolic calcium level have been identified. Cytosolic calcium level was found to increase in lymphocytes in response to a high-salt diet in salt-sensitive individuals with hypertension, yet the identification of a circulating inhibitor of sodium-potassium--dependent adenosine triphosphatase remains elusive. Dietary intervention trials of salt restriction in patients with hypertension are generally disappointing. Active research is elucidating the role of sodium intake and hypertension at all levels. The data to date, however, still do not allow sweeping conclusions or generalizations.