A reduced NaCl intake for the general population of the world has been recommended to reduce the overall blood pressure level and hence to reduce the overall incidence of cardiovascular disease. A high NaCl diet convincingly contributes to elevated arterial pressure in humans and animal models of hypertension. Among individuals there is considerable variability of blood pressure responsiveness to NaCl intake. In normotensive as well as hypertensive subjects, blood pressure can be judged to be salt sensitivity (SS) when observed to vary directly and substantially with the net intake of NaCl. The prevalence of SS in normotensive adults in the U.S. ranges from 15% to 42% and in hypertensive adults from 28% to 74%. SS is a risk factor for hypertension and may be an important marker in the identification of children for hypertension prevention programs. High NaCl intakes produce expansion of the extracellular fluid volume and thus increase blood pressure. Nonchloride salts of sodium does not expand the extracellular fluid volume and does not alter blood pressure. Blood pressure response to NaCl may be modified by other components of the diet. Low dietary intakes of potassium or calcium augment NaCl-induced increases of blood pressure. Conversely, high dietary intakes of potassium or calcium attenuate NaCl-induced hypertension. A greater intakes of potassium or calcium may prevent or delay the occurrence of hypertension. SS occurs when dietary potassium is even marginally deficient but is dose-dependently suppressed when dietary potassium is increased within its normal range. Orally administered KHCO$_3$, abundant in fruits and vegetates, but not KCl has a calcium-retaining effect which may contributed to its reversal of pressor effect of dietary NaCl. Since nutrients other than NaCl also affect blood pressure levels, a reduced NaCl intake should be only one component of a nutritional strategy to lower blood pressure.