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(Chest. 1980;78:140-149.)
© 1980 American College of Chest Physicians

Biochemical Basis for Contraction of Vascular Smooth Muscle

David J. Hartshorne Ph.D.1

1 From the Departments of Biochemistry, and Nutrition and Food Science, Muscle Biology Group, University of Arizona, Tucson

Some of the current facts and theories concerning the contractile mechanism in smooth muscle are summarized. The review is divided into two major sections. One deals with the components of the contractile apparatus (the thick and thin filaments), and the protein components of each filament type are described briefly. The other is devoted to the Ca2+-dependent mechanism of regulation in smooth muscle, and this is restricted to those components that control the activity of the contractile apparatus. There are basically two theories that have been proposed as the regulatory mechanism in smooth muscle. One theory is that the regulatory mechanism is located on the thin filaments and is functional via some modification of the thin filament proteins. This system is termed leiotonin. The second theory is that regulation is achieved by the phosphorylation and dephosphorylation of the light chains of myosin. Since the latter theory represents the author's bias and in general is more widely accepted, it is considered in more detail. A cyclic scheme is presented to illustrate the role of the myosin light chain kinase in the activation and contraction of smooth muscle and the role of the myosin light chain phosphatase in the relaxation process.







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Copyright © 1980 by the American College of Chest Physicians.