Normal pregnancy is associated with significant hemodynamic changes in the cardiovascular system in order to meet the metabolic demands of mother and fetus. These changes include increased cardiac output, decreased vascular resistance, and vascular remodeling in the uterine and systemic circulation. Preeclampsia (PE) is a major complication of pregnancy characterized by proteinuria and hypertension. Several risk factors have been implicated in the pathogenesis of PE including genetic and dietary factors. Ca 2+ is an essential dietary element and an important regulator of many cellular processes including vascular function. The importance of adequate dietary Ca 2+ intake during pregnancy is supported by many studies. Pregnancy-associated changes in Ca 2+ metabolism and plasma Ca 2+ have been observed. During pregnancy, changes in intracellular free Ca 2+ concentration ([Ca 2+ ] i ) have been described in red blood cells, platelets and immune cells. Also, during pregnancy, an increase in [Ca 2+ ] i in endothelial cells (EC) stimulates the production of vasodilator substances such as nitric oxide and prostacyclin. Normal pregnancy is also associated with decreased vascular smooth muscle (VSM) [Ca 2+ ] i and possibly the Ca 2+ -sensitization pathways of VSM contraction including protein kinase C, Rho-kinase, and mitogen-activated protein kinase. Ca 2+ -dependent matrix metalloproteinases could also promote extracellular matrix degradation and vascular remodeling during pregnancy. Disruption in the balance between dietary, plasma and vascular cell Ca 2+ may be responsible for some of the manifestation of PE including procoagulation, decreased vasodilation, and increased vasoconstriction and vascular resistance. The potential benefits of Ca 2+ supplements during pregnancy, and the use of modulators of vascular Ca 2+ to reduce the manifestations of PE in susceptible women remain an important area for experimental and clinical research.