Figure 1017

Electron micrograph of smooth muscle cells. This electron micrograph shows parts of three smooth muscle cells. The nucleus of one cell is in the lower part of the micrograph. The bulk of the cytoplasm is occupied by thin (actin) filaments, which are just recognizable at this magnification. The a-actinin-containing cytoplasmic densities, or dense bodies, are visible among the myofilaments (arrows). Elements of the sarcoplasmic reticulum (SR) and the pinocytotic vesicles (PV) are also indicated. The other two cells in the middle and upper part of the micrograph possess visible gap junctions (GJ) that allow communication between adjacent cells. The small dark particles are glycogen. x25,000. Inset. Enlargement of the gap junction. Note the presence of pinocytotic vesicles, x 35,000.

dense bodies, may also appear as irregular linear structures. In fortuitous sections, they exhibit a branching configuration consistent with a three-dimensional anastomosing network that extends from the sarcolemma into the interior of the cell (Fig. 10.18).

Contraction of smooth muscle is regulated by the Ca2+-calmodulin/myosin light chain kinase system

A modified version of the sliding filament model described on page 256 can explain contraction in both stri ated and smooth muscle (Fig. 10.19). As in striated muscle, contraction is initiated by an increase in the Ca2+ concentration in the cytosol, but the contraction does not act through a troponin-tropomyosin complex on the thin filament. Rather, in smooth muscle, an increase in Ca2+ concentration stimulates a myosin light chain kinase to phos-phorylate one of the two light chains of myosin. The phosphorylation reaction is regulated by a Ca2^-calmodulin complex. When the light chain of myosin is phos-phorylated, the myosin head attaches to actin and produces contraction. When it is dephosphorylated, the

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