Regulation of Contraction and Relaxation in Arterial Smooth Muscle

Rembold, Christopher M.

Division of Cardiology, Departments of Internal Medicine and Physiology, University of Virginia School of Medicine, Charlottesville, Va.

Address for reprints: Christopher M. Rembold, MD, Box 146, Division of Cardiology, University of Virginia Health Sciences Center, Charlottesville, VA 22908.

Supported by a grant from the Lucille P. Markey Charitable Trust in addition to support from grant RO1-HL-38918 from the National Institutes of Health and the American Heart Association, Virginia Affiliate, Inc. C.M.R. is a Lucille P. Markey scholar.

Received December 13, 1991; accepted in revised form February 19, 1992.

Hypertension 20(2):p 129-137, August 1992.

Intracellular calcium concentration ([Ca−²⁺]₁)dependent activation of myosin light chain kinase and its phosphorylation of the 20-kd light chain of myosin is generally considered the primary mechanism responsible for regulation of contractile force in arterial smooth muscle. However, recent data suggest that the relation between [Ca²⁺]₁, and myosin light chain phosphorylation is variable and depends on the form of stimulation. The dependence of myosin phosphorylation on [Ca²⁺]₁, has been termed the “[Ca²⁺]₁, sensitivity of phosphorylation.” The [Ca²⁺]₁, sensitivity of phosphorylation is “high” when relatively small increases in [Ca²⁺]₁, induce a large increase in myosin phosphorylation. Conversely, the [Ca²⁺]₁, sensitivity of phosphorylation is “low” when relatively large increases in [Ca²⁺]₁, are required to induce a small increase in myosin phosphorylation. There are two proposed mechanisms for changes in the [Ca²⁺]₁, sensitivity of phosphorylation: Ca²⁺-dependent decreases in the [Ca²⁺]₁, sensitivity of phosphorylation induced by phosphorylation of myosin light chain kinase by Ca²⁺-calmodulin protein kinase II and agonist-dependent increases in the [Ca²⁺]₁, sensitivity of phosphorylation by inhibition of a myosin light chain phosphatase. I will review the proposed mechanisms responsible for the regulation of [Ca²⁺]₁, and the [Ca²⁺]₁, sensitivity of phosphorylation in arterial smooth muscle.