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The Debate That Begs the Bigger Question

Arch Intern Med. 2001;161:507-510.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

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.

BACKGROUND

There is an escalating debate about whether a high salt (sodium chloride) intake raises blood pressure and causes essential hypertension in the general population.^{1, 2, 3, 4, 5, 6, 7} At the center of the debate is the proposition that in industrialized nations a subset of the population is salt sensitive, and in salt-sensitive persons a high salt . . . [Full Text of this Article]

THE ROOTS OF THE SALT DEBATE

THE ROLE OF THE KIDNEYS IN SALT-INDUCED BLOOD PRESSURE ELEVATION

THE EFFECT OF A HIGH SALT INTAKE ON PARAMETERS OTHER THAN BLOOD PRESSURE

DIETARY POTASSIUM INTAKE, HYPERTENSION, AND STROKE

PLATELETS AND SALT SENSITIVITY

CONCLUSIONS

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