1. We propose the following model of Ca 2+ mobilization by noradrenaline in vascular smooth muscle. Upon receptor occupation Ca 2+ from a labile small intracellular store on the inner plasmalemma is released. This Ca 2+ does not function as activator Ca 2+ but triggers Ca 2+ release from the sarcoplasmic reticulum (Ca 2+ -induced Ca 2+ release). 2. Simultaneously Ca 2+ from an extracellularly bound store (on the external surface of the plasmalemma) is dislodged, which enters the cell through receptor linked channels. 3. These processes are responsible for the early ‘phasic’ component of the noradrenaline contraction. In addition, Ca 2+ from the free extracellular Ca 2+ pool enters through receptor operated channels, supporting the maintained tension development.