Abstract
DIETARY sodium and potassium seem to exert blood pressure–independent effects on cardiovascular morbidity and mortality. These effects have not received their due attention in the debate about salt sensitivity. Epidemiological and experimental data suggest a direct connection between dietary sodium intake and left ventricular hypertrophy and between sodium and potassium intake and stroke. The strong dependency of platelet calcium homeostasis on cellular and systemic sodium and potassium regulation along with the evidence that a high salt intake augments platelet reactivity supports the concept that platelets are an important link between dietary sodium and potassium intake and occlusive stroke.