Low-density (LDL) and high-density (HDLj) lipoproteins dose-dependently activate phosphoinositide turnover and elevate cytosolic free Ca 2+ concentrations ([Ca 1+ ]|) in cultured vascular smooth muscle cells (VSMCs) from either human (microarterioles and aorta) or rat (aorta) sources. High-performance liquid chromatography analysis of cell extracts revealed comparable spectra of inositol phosphate isomers generated in response to either LDL, HDL,, or angiotensin II (Ang II 10 Epidemiologic studies also show that hypertension is a major risk factor for development of atherosclerosis. 4 Different hypotheses have been proposed to explain the association between the two diseases, with the common etiologic denominators being either disturbances in plasma lipoprotein concentrations and cellular cholesterol homeostasis, 5 intracellular calcium overload, 6 or altered responses to growth factors and vasoregulatory hormones.1 -3 These theories are not mutually exclusive, however, and linkage between the latter two is predictable because growth factors and vasoregulatory hormones are known to mobilize intracellular calcium. The relation between lipoprotein/cholesterol disturbances and the calcium-based or agonist growth factor-based theories is less conspicuous, but it