The control of vasomotion is a central issue in blood pressure regulation and is a primary goal of antihypertensive therapy. Calcium is the final messenger in the contractile mechanism of vascular smooth and cardiac muscle. Vasoconstrictor agents enhance the entry of Ca++ into vascular myocytes; vasodilators usually depress it. The most recent findings, based on direct measures of intracellular Ca++, have also highlighted the importance of calcium-sensitization mechanisms: vasoconstrictors sensitize the contractile apparatus to Ca++; vasodilators have an opposite effect. Cell calcium control alterations have been reported in different forms of hypertension. An increase in vascular myoplasmic Ca++ and a higher rate of calcium influx through specific, dihydropiridine-sensitive calcium channels have been found in genetic or secondary animal models. In hypertensive patients, an elevation of cytoplasmic Ca++ was noted in the platelets. Since Ca++ is a ubiquitous intracellular messenger, these changes may have profound implications for the pathophysiology of hypertension.