In vascular smooth muscles, neurotransmitters or autacoids produce contraction through activation of Ca2(+)-influx and release of Ca2+ from intracellular store sites. These agonists appear to activate Ca2(+)-influxes in both voltage-dependent and voltage-independent manners. The release of Ca2+ is though to be linked to the action of inositol 1,4,5-trisphosphate. The phosphorylation of myosin light chain may be the mechanism for the Ca2(-+)-induced contraction in smooth muscles. Some agonists only transiently increase cellular Ca2+ and the phosphorylation of myosin, but they produce a sustained contraction in various vascular tissues. Hence, additional high Ca2(+)-sensitive mechanisms are no doubt involved in the contraction of vascular smooth muscle. In the present article, attention will be directed to the mechanisms and agonist-induced contraction in arterial smooth muscle.