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Dietary salt, intracellular ion homeostasis and hypertension secondary to early-stage kidney disease.

Abnormal salt metabolism plays a central role in the pathogenesis of hypertension caused by early-stage renal disease. The mechanisms by which alterations in salt balance and the vasoconstrictor state are related are unclear. We studied the effects of three different salt diets (3, 6-9 and 12 g sodium chloride) on cellular ion homeostasis in platelets in 20 patients with renal hypertension. Compared to normal subjects, patients with renal hypertension had raised cytosolic sodium and calcium concentrations. The platelet sodium pump activity was significantly depressed and calcium ATPase activity increased. These abnormalities of cellular ion metabolism were aggravated by salt overload. On the other hand, dietary salt restriction tended to normalise these parameters. The data presented indicate that a circulating inhibitor of the sodium pump plays a central role in the pathogenesis of salt-induced renal hypertension and that the final common pathway of hypertension secondary to early-stage parenchymal renal disease is an elevation of resting cytosolic calcium followed by an elevation of peripheral vascular resistance.