Ca2+ regulation of the thin filaments: biochemical mechanism and physiological role.

Abstract

The control of blood flow and blood pressure is primarily a question of the control of the contractility of the smooth muscle cells in blood vessel walls. The contractile machinery of smooth muscle cells is made up of filaments of the contractile proteins myosin (thick filaments) and actin (thin filaments), the interaction of which generates force and shortening at the expense of MgATP hydrolysis. The contractile proteins are associated with regulatory proteins which control the actin-myosin interaction in response to changes in the Ca2+ concentration in the surrounding cytoplasm. One site of action of Ca2+ on the contractile apparatus: Ca2 +-dependent phosphorylation of myosin by a calmodulin-dependent myosin light chain kinase, leading to activation, has been demonstrated and studied extensively. The other site of Ca2+ action: Ca2+ regulation of the thin filaments, has now been identified in many smooth muscles and we have studied it in some detail in vascular smooth muscle (Marston & Smith, 1985). We have developed a procedure to isolate native thin filaments from sheep aorta and many other smooth muscle