The AT1 receptor mediates many biological effects of the renin angiotensin system such as vasoconstriction and cell proliferation. The expression level of the AT1 receptor is subjected to various pathophysiological influences. Insulin, which is elevated in the metabolic syndrome, induces a overexpression of vascular AT1 receptors leading to an enhanced biological efficacy of angiotensin II. This heterologous regulation of the AT1 receptor by insulin may explain the fact that the metabolic syndrome is frequently associated with hypertension and atherosclerosis.