The contractile state of vascular smooth muscle cells (VSMCs) is a major determinant for the blood pressure and therefore a key target for vasorelaxant drugs. The contractile stage of VSMCs is regulated by membrane potential-dependent Ca²⁺-entry through Ca²⁺-channels and Ca²⁺ release from intracellular Ca²⁺ stores. The physiological consequences of the modulation of the membrane potential are difficult to investigate because electrical field stimulation can only be used to initiate action potentials but not for long lasting modulations of the membrane potential. To overcome these technical limitations and to better understand mechanisms underlying graded depolarization of VSMCs we have analyzed transgenic mice that express the light-gated cation channel channelrhodopsin2 (ChR2) fused to EYFP under control of the chicken-b-actin promoter (Nat Methods. 2010; 7:897–900). VSMCs in the vascular wall of the aorta showed membrane bound EYFP fluorescence indicating ChR2 expression. The function of ChR2 in aortic VSMCs was investigated using isometric force measurements of aortic rings with a wire-myograph. Illumination of the rings with blue light (475nm, 2.7mW/mm²) reliably induced contractions with a force generation comparable to noradrenalin (10mM) stimulation but with much faster on- (< 800 ms) and off-kinetics (< 2.5 s) and could be maintained up to 10 min. Light illumination of vessels from wild-type mice or transgenic mice expressing EGFP only did not induce contractions. We conclude that ChR2 expression can be used for light-induced contraction of VSMCs with high spatio-temporal precision. Thus, this is a new and powerful technique to analyze membrane-potential dependent mechanisms in VSMCs.