Although there is much circumstantial and some direct clinical evidence suggesting that a high consumption of salt predisposes patients to the development of essential hypertension, the mechanism by which such consumption causes high blood pressure is not clear. It has been suggested that due to an inherited abnormality in renal sodium excretion, high salt intake triggers an increase in the levels of sodium transport inhibitor. Although this may help to restore sodium balance, it may also increase the concentration of intracellular sodium in arteriolar smooth muscle and, thereby, stimulate smooth muscle reactivity. It has been shown that intra-arterial infusion of calcium channel blockers into the forearm produces an enhancement of forearm blood flow that is proportional to the degree of hypertension. Other studies have demonstrated a linear relationship between the degree of hypertension and the magnitude of blood pressure reduction following treatment with a calcium channel blocker. These clinical findings, combined with evidence from studies in animals, suggest that a functionally abnormal response of smooth muscle cells to calcium channel blockers occurs as blood pressure increases. Whether this functional abnormality is related to an increased level of intracellular calcium and/or inhibition of the sodium pump is not known. The short-term blood pressure lowering effect of nifedipine appears to be enhanced when sodium intake is increased.