Human salusin- α and salusin- β are related peptides produced from prosalusin. Bolus injection of salusin- β into rats induces more profound hypotension and bradycardia than salusin- α . Central administration of salusin- β increases blood pressure via release of norepinephrine and arginine-vasopressin. Circulating levels of salusin- α and salusin- β are lower in patients with essential hypertension. Salusin- β exerts more potent mitogenic effects on human vascular smooth muscle cells (VSMCs) and fibroblasts than salusin- α . Salusin- β accelerates inflammatory responses in human endothelial cells and monocyte-endothelial adhesion. Human macrophage foam cell formation is stimulated by salusin- β but suppressed by salusin- α . Chronic salusin- β infusion into apolipoprotein E-deficient mice enhances atherosclerotic lesions; salusin- α infusion reduces lesions. Salusin- β is expressed in proliferative neointimal lesions of porcine coronary arteries after stenting. Salusin- α and salusin- β immunoreactivity have been detected in human coronary atherosclerotic plaques, with dominance of salusin- β in macrophage foam cells, VSMCs, and fibroblasts. Circulating salusin- β levels increase and salusin- α levels decrease in patients with coronary artery disease. These findings suggest that salusin- β and salusin- α may contribute to proatherogenesis and antiatherogenesis, respectively. Increased salusin- β and/or decreased salusin- α levels in circulating blood and vascular tissue are closely linked with atherosclerosis. Salusin- α and salusin- β could be candidate biomarkers and therapeutic targets for atherosclerotic cardiovascular diseases.