Pharmacomechanical Coupling in Vascular Smooth Muscle Cells -An Overview -

Abstract

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 thought 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.