ArticleJournal of muscle research and cell motility1993
Models of the mechanism for crossbridge attachment in smooth muscle.
Article in Journal of muscle research and cell motility, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- The vital role for nitric oxide in intraocular pressure homeostasis.Progress in retinal and eye research · 2021Review
- Cross-bridge apparent rate constants of human gallbladder smooth muscle.Journal of muscle research and cell motility · 2011Article
- Cellular and molecular mechanisms regulating vascular tone. Part 1: basic mechanisms controlling cytosolic Ca2+ concentration and the Ca2+-dependent regulation of vascular tone.Journal of anesthesia · 2007Review
- The role of MgADP in force maintenance by dephosphorylated cross-bridges in smooth muscle: a flash photolysis study.Biophysical journal · 1995Article
- Myosin light chain kinase-regulated endothelial cell contraction: the relationship between isometric tension, actin polymerization, and myosin phosphorylation.The Journal of cell biology · 1995Article
- Effects of inorganic phosphate on cross-bridge kinetics at different activation levels in skinned guinea-pig smooth muscle.The Journal of physiology · 1995Article
- The variable coupling between force and myosin light chain phosphorylation in Triton-skinned chicken gizzard fibre bundles: role of myosin light chain phosphatase.Pflugers Archiv : European journal of physiology · 1995Article
- Flash photolysis studies of relaxation and cross-bridge detachment: higher sensitivity of tonic than phasic smooth muscle to MgADP.Journal of muscle research and cell motility · 1993Article
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Authors and funding
2 authors.
Funding
Abstract
The mechanism responsible for formation of attached, dephosphorylated crossbridges (latchbridges) in smooth muscle is controversial. Myosin light chain phosphorylation may be obligatory for crossbridge attachment; if this were the case, latchbridges would arise solely by dephosphorylation of attached, phosphorylated crossbridges. Alternatively, the presence of attached crossbridges could induce cooperative activation by allowing dephosphorylated crossbridges to attach to the thin filament. We evaluated whether four-state models based on dephosphorylation and/or cooperativity-regulated attachment could quantitatively predict smooth muscle contractile behaviour. Five quantitative models for transitions between crossbridge states were developed. Mechanisms for latchbridge formation included: (1) dephosphorylation, (2) cooperativity-regulated attachment dependent only on attached, phosphorylated crossbridges, (3) cooperativity-regulated attachment dependent on all attached crossbridges, (4) dephosphorylation and cooperativity-regulated attachment dependent only on attached, phosphorylated crossbridges, and (5) dephosphorylation and cooperativity-regulated attachment dependent on all attached crossbridges. All five models approximated the time course of contraction and the dependence of steady-state stress on myosin phosphorylation in the swine carotid artery. In the two models that had cooperative attachment regulated by all attached crossbridges, small increases in the rate constant for cooperativity-regulated attachment resulted in positive feedback and irreversible contraction. We suggest that a number of four-state crossbridge models can predict contractile behaviour in arterial smooth muscle. Potentially, latchbridges could be formed by both dephosphorylation and cooperativity-regulated attachment. If cooperativity-regulated latchbridge attachment does exist in smooth muscle, we suggest that it should be dependent only on the number of phosphorylated crossbridges rather than all attached crossbridges.
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