Depending on their anatomical origin, the responsiveness of vascular smooth muscle cells to alpha 1- and alpha 2-selective adrenergic agonists and antagonists varies. In most large arteries, the postjunctional alpha-adrenoceptors appear to belong mainly to the alpha 1-subtype; in large veins, and possibly in resistance vessels, the vascular smooth muscle cells also contain alpha 2-adrenoceptors that can trigger the contractile process. In the large veins, lower concentrations of norepinephrine cause mainly activation of the alpha 2-adrenoceptors, while higher amounts of the transmitter also recruit alpha 1-adrenoceptors. The Ca2+-entry blocker verapamil inhibits more readily contractions due to alpha 1- than those caused by alpha 2-selective adrenergic agonists, suggesting a link between the former and the entry of extracellular Ca2+ in the vascular smooth muscle cells.