Myosin Phosphorylation and Crossbridge Regulation in Arterial Smooth Muscle

Regulation of rascuiar resistance is generally explained in terms of neural, hormonal, metabolic, and myogenic factors altering intracellular calcium [Ca] in vascular smooth muscle. Ca acts as a second messenger regulating the number of active crossbridges and force generation by binding to a myofilament regulatory protein. A search for the Ca-blndlng regulatory protein in arterial smooth muscle has uncovered what appears to be a new type of regulation. In addition to its interaction with an undefined Cabinding site which determines force development, Ca stimulates phosphorylation of the crossbridges. Phosphorylated crossbridges cyde more rapidly than dephospborylated crossbridges in the presence of Ct + + . Some known characteristics of the myosin light chain kinase/pbosphatase system and the effects of crossbridge phosphorylation on the mechanics of arterial smooth muscle are described. Chronic alterations in this system have potential effects on vascular resistance and merit investigation in studies of arterial smooth muscle from hypertensive animal models. (Hypertension 4 (suppl II): II-3-II-7, 1982)