Abstract
Smooth muscle cells can regulate both their rate of stress development and the level of maintained stress. Agonist-induced steady-state stress was dependent on changes in aequorin-estimated myoplasmic [Ca2+] in the range of 120-190 nM. Higher levels of [Ca2+] were observed only transiently after stimulation and correlated with higher levels of myosin phosphorylation and faster stress development. A single regulatory system (Ca2+-dependent myosin light-chain phosphorylation) appears to control both mean crossbridge cycling rates (rate of contraction or shortening velocity) and the number of attached crossbridges (stress).
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