Industrially processed food contributes with 75 % of total daily salt intake and recent long term trials controlling the actual salt intake by providing all foods and drinks for study participants have shown that the mean blood pressure lowering effect of a 6 gram reduction of salt intake is approximately 6/3 mmHg, i.e. an effect comparable to antihypertensive pharmacological monotherapy. Importantly, whereas most individuals are salt sensitive, the degree of salt sensitivity (the degree of blood pressure reduction following a lowering of salt intake) differs between individuals. A low plasma concentration of renin predicts high salt sensitivity. This suggests that enhanced renal tubular sodium reabsorption, which suppresses renin release from the juxtaglomerular apparatus, contributes to high degree of salt sensitivity. Monogenic rare forms of human hypertension are predominantly caused by mutations leading to increased tubular sodium reabsorption through the epithelial amiloride sensitive sodium channel (ENaC) which leads to suppression of renin release and severe salt sensitive hypertension. Whereas common forms of hypertension and population blood pressure variation is not influenced by genetic variation of ENaC, common genetic variation of the key regulatory protein of ENaC, the Neural Precursor Cell Expressed Developmentally Down-regulated 4-Like (NEDD4L) is associated with higher population blood pressure, increased salt sensitivity, reduced plasma renin concentration and increased risk of cardiovascular disease. Based on recent results, this talk will review the effects of salt intake on blood pressure as well as determinants of salt sensitivity, blood pressure and its long term cardiovascular consequences in man.