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Latch-bridge model in smooth muscle: [Ca2+]i can quantitatively predict stress.
1Department of Internal Medicine, University of Virginia Health Science Center, Charlottesville 22908.
The American Journal of Physiology
|August 1, 1990
Summary
Calcium (Ca2+) levels directly regulate smooth muscle contraction. Changes in myoplasmic Ca2+ quantitatively predict myosin light chain kinase activity, phosphorylation, and force, explaining muscle contraction and relaxation.
Area of Science:
- Physiology
- Muscle Biology
- Biochemistry
Background:
- Smooth muscle contraction is regulated by Ca2+-dependent cross-bridge phosphorylation via myosin light chain kinase.
- A four-state cross-bridge model explains smooth muscle contraction and latch state (high force, low cycling).
Purpose of the Study:
- To test if myoplasmic Ca2+ changes quantitatively predict myosin kinase activity, phosphorylation, and force production.
- To validate the role of Ca2+ and myosin light chain kinase in smooth muscle function.
Main Methods:
- Used aequorin to estimate myoplasmic Ca2+ concentration.
- Measured isometric stress production and cross-bridge phosphorylation.
- Stimulated smooth muscle with histamine and angiotensin II, and used cyclic AMP for relaxation.
Main Results:
- Aequorin-estimated myoplasmic Ca2+ changes quantitatively predicted phosphorylation and isometric stress.
- This correlation held true during agonist stimulation and cyclic AMP-mediated relaxation.
- Results support the sufficiency of Ca2+ and myosin light chain kinase in regulating smooth muscle tone.
Conclusions:
- Myoplasmic Ca2+ concentration is a key determinant of smooth muscle contraction and relaxation.
- The proposed four-state model, driven by Ca2+-dependent myosin kinase activity, effectively explains smooth muscle mechanics.
- Agonist-induced changes in swine carotid arterial smooth muscle can be explained by Ca2+ and myosin light chain kinase activation.