This chapter reviews the evidence in favor of biological associations of both sodium and potassium intake with cardiovascular risk, addressing the possible mechanisms whereby sodium contributes to while potassium may protect from the development of cardiovascular disease through their effects on blood pressure (BP) and possibly beyond. Left ventricular hypertrophy, another expression of organ damage and independent predictor of cardiovascular morbidity and mortality, was positively associated with sodium intake in two studies apparently through the increase in BP. Urinary albumin excretion, an expression of subclinical organ damage and risk factor for the development and progression of renal disease, is associated with sodium intake. Many studies in animal models suggested that a high potassium intake may reduce cardiovascular organ damage and counteract the increase in cardiovascular event rates caused by a high sodium intake, even independently from its effect on BP.