Red-Cell Sodium-Lithium Countertransport and Essential Hypertension

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Abstract
To the Editor: The paper by Woods et al. (March 11 issue)1 provides additional support for the proposal by Canessa et al.2 that overactivity of the red-cell transport pathway mediating sodium–lithium exchange may be a genetic marker for essential hypertension. Under physiologic conditions, in the absence of lithium, this pathway mediates ouabain-insensitive, 1:1 sodium-sodium exchange.3 Thus, variations in the activity of this pathway are without impact on intracellular electrolyte content, and the possible role of this type of abnormality in sodium transport in the pathogenesis of essential hypertension has been particularly obscure.I wish to suggest the possibility that in . . .