Vascular smooth muscle shows both plasticity and heterogeneity with respect to Ca(2+) signaling. Physiological perturbations in cytoplasmic Ca(2+) concentration ([Ca(2+)](i)) may take the form of a uniform maintained rise, a transient uniform [Ca(2+)](i) elevation, a transient localized rise in [Ca(2+)](i) (also known as spark and puff), a transient propagated wave of localized [Ca(2+)](i) elevation (Ca(2+) wave), recurring asynchronous Ca(2+) waves, or recurring synchronized Ca(2+) waves dependent on the type of blood vessel and the nature of stimulation. In this overview, evidence is presented which demonstrates that interactions of ion transporters located in the membranes of the cell, sarcoplasmic reticulum, and mitochondria form the basis of this plasticity of Ca(2+) signaling. We focus in particular on how the junctional complexes of plasmalemma and superficial sarcoplasmic reticulum, through the generation of local cytoplasmic Ca(2+) gradients, maintain [Ca(2+)](i) oscillations, couple these to either contraction or relaxation, and promote Ca(2+) cycling during homeostasis.