Pharmacomechanical coupling in vascular smooth muscle cells--an overview.
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.
Itoh
T
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Department of Pharmacology, Faculty of Medicine, Kyusyu University, Fukuoka, Japan.
D000595:Amino Acid Sequence; D000818:Animals; D001696:Biomechanical Phenomena; D002118:Calcium / Q000502:physiology*; D008969:Molecular Sequence Data; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000502:physiology; D009218:Myosins / Q000378:metabolism; D010766:Phosphorylation; D015290:Second Messenger Systems / Q000502:physiology
D009218:Myosins; D002118:Calcium