SMOOTH MUSCLE

Light Microscopic Structure

Smooth muscle cells are elongated, spindle-shaped cells (Fig. 5-1). Each cell contains a single, centrally located nucleus. The cells range from 5 to 20 µm in diameter and from 20 µm to 1 mm or more in length. The cytoplasm of smooth myocytes is acidophilic.

Within a tissue section, the cross-sectional size of cells is highly variable due to the tapered shape of the cells. Many cross sections of the cell lack nuclear profiles because of the extent of the cell beyond the central nuclear region (Fig. 5-1A).

FIGURE 5-1 Smooth muscle. A. Cross section. B. Longitudinal section. The central myocyte nuclei (solid arrows) are absent in several cross sections due to sectional geometry. The tip of a spindle-shaped cell is visible at the dotted arrow. Fibroblast nuclei (open arrow) are dark and smaller than smooth muscle nuclei. Hematoxylin and eosin (×490).

Individual myocytes are surrounded by a fine network of reticular fibers, blood vessels, and nerves. In smooth muscle, reticular fibers are produced by myocytes rather than fibroblasts. Although the connective tissue is analogous to the endomysium of skeletal muscle described below, it is not termed as such.

Fine Structure

The cytoplasm of the smooth muscle myocyte contains numerous myofilaments in various orientations (Figs. 5-2 and 5-3). Thin myofilaments of smooth muscle contain actin and tropomyosin but lack troponin, which is present in skeletal and cardiac muscle. Thick myofilaments, composed of myosin-II, are sparse. The thick and thin myofilaments are not arranged in a highly ordered pattern as in striated muscle. Dense bodies in the cytoplasm and the cell membrane serve as anchor sites for the myofilaments. Intermediate filaments (desmin and vimentin) further link the dense bodies into a meshwork array. The myofilament attachment sites on the cell membrane also form junctions that connect adjacent cells.

Numerous pear-shaped invaginations (caveolae) and vesicles are present along the cell membrane and are believed to play a role in calcium transport (Figs. 5-2 and 5-3). Transverse T tubules found in striated muscle are lacking and smooth endoplasmic reticulum is sparse. Gap junctions, which allow for cell coupling, occur at frequent periodic sites in the cell membrane. Other cellular organelles, including mitochondria, Golgi complex, rough endoplasmic reticulum (rER), and free ribosomes, are located near the nucleus. Each myocyte is surrounded by a basal lamina, except at intercellular junctions (Fig. 5-3).

Contraction

The contractile apparatus of smooth muscle is capable of greater shortening in length and more sustained contractions than that of striated muscle. Contraction is governed by the phosphorylation of the myosin-II molecule in contrast to striated muscle, which is regulated by a troponin–tropomyosin complex described below.

The contraction sequence begins with an increase of calcium in the smooth muscle cell cytoplasm. Calcium increases by entering the cell through voltage-dependent calcium channels in the cell membrane or by inositol 1,4,5-triphosphate (IP₃)-induced release of calcium from the smooth endoplasmic reticulum. The rise in cytosolic calcium leads to subsequent binding of the calcium to calmodulin. The calcium–calmodulin complex then interacts with myosin light-chain kinase, which initiates phosphorylation of myosin-II and interaction between the actin and myosin-II myofilaments. The overall process leading to actin–myosin interaction is longer when compared with other muscle types, which results in the relatively slow contraction of smooth muscle.

Hormones that act via cyclic adenosine monophosphate (cAMP) can affect smooth muscle contraction. cAMP activates myosin light-chain kinase, leading to phosphorylation of myosin and cell contraction. Estrogen increases cAMP and subsequently smooth muscle contraction, while progesterone decreases cAMP, resulting in decreased smooth muscle contraction.

Contraction of smooth muscle is involuntary. Innervation is both parasympathetic and sympathetic, and the effects of neural input on smooth muscle are variable. Unitary smooth muscle, found in the wall of visceral organs, behaves as a syncytium that contracts in a networked fashion. Cells of this arrangement of smooth muscle are extensively connected by gap junctions but sparsely innervated. In contrast, multiunit smooth muscle, found in the iris of the eye, is capable of precise contractions due to individual innervation of each myocyte. The multiunit myocytes lack gap junctions, resulting in reduced coordinated communication between cells.

Myogenesis, Hypertrophy, and Regeneration

Smooth muscle tissue increases in size by both hypertrophy (increase in size) and hyperplasia (increase in number) of myocytes. New smooth muscle cells can form through mitosis or by derivation from pericytes. Formation of new myocytes is limited, so healing of smooth muscle is mainly through connective tissue scar formation.

SKELETAL MUSCLE

Skeletal muscle myocytes are elongated cells that range from 10 to 110 µm in diameter and can reach up to 50 cm in length. These fibers are derived from the prenatal fusion of many individual mononuclear myoblasts. As a result of the fusion, a single myocyte contains multiple oval nuclei, which are peripherally located within the cell (Fig. 5-4). When viewed in longitudinal section, transverse striations are present as alternating light and dark bands. In transverse section, the myocyte has an angular outline and a stippled cytoplasm (Fig. 5-5). Peripheral nuclei may be absent in some planes of the cross section of the myocyte. The surrounding cell membrane is visible at higher magnification.

FIGURE 5-2 The smooth muscle cell has a centrally located nucleus surrounded by cytoplasm containing myofilaments in various orientations. The contractile myofilaments anchor into dense bodies on the cell membrane and within the cytoplasm of the smooth muscle cell. When the myofilaments contract, the cell shortens (lower diagram). Numerous caveolae, vesicles, and gap junctions are present along the cell membrane.

FIGURE 5-3 Electron micrograph of a cross-sectioned smooth muscle cell. The nucleus (N) is centrally located, and the cytoplasm contains numerous myofilaments. Electron-dense bodies (*) serve as attachment sites for the myofilaments. Numerous caveolae (arrowheads) are present along the plasma membrane of an adjacent cell. The basal laminae (L) are visible between the two cells and appear fused at points (×23,900). (Courtesy of W. S. Tyler.)

Each muscle cell contains myofibrils, which form the dots in cross sections of the fiber at the light microscopic level (Fig. 5-6). The myofibrils are cylindrical and 1 to 2 µm in diameter. Individual myofibrils are composed of thick and thin myofilaments, which are responsible for contraction. The myofibrils align in a longitudinal direction to create the light and dark banding pattern of the myocyte. Thick and thin myofilaments overlap in the darker A band (anisotropic), whereas only thin myofilaments are present in the lighter I band (isotropic). The myofibrils are connected by intermediate filaments of desmin and vimentin, such that the light and dark bands of all myofibrils within a fiber are in register.

FIGURE 5-4 Skeletal muscle, longitudinal section. Notice the cross-striations and the nuclei located in the periphery of the myocytes. Hematoxylin and eosin (×435).

Satellite cells are spindle-shaped cells located adjacent to the cell membrane of the myocyte and within its basement membrane. Their nuclei are heterochromatic in contrast to the lighter-staining nuclei of the myocyte. Satellite cells are best recognized with electron microscopy. They are thought to represent a population of inactive myoblasts, which can be activated upon injury to initiate regeneration of muscle fibers.

FIGURE 5-5 Skeletal muscle, cross section. The nuclei in the sparse endomysium (arrows) belong to either fibroblasts or satellite cells. Hematoxylin and eosin (×435).

FIGURE 5-6 The myofibrils of skeletal muscle are comprised of myofilaments. Smooth endoplasmic reticulum surrounds each myofibril and forms terminal cisternae near the T tubule. T tubules extend into the cytoplasm from the cell membrane and surround the myofibrils at the A–I junction. A T tubule plus two terminal cisternae form a triad structure. Peripheral nuclei of the skeletal muscle myofiber are not shown in this illustration.

Individual myocytes are bound together into primary bundles or fascicles (Fig. 5-7). Within a fascicle, an individual myocyte is surrounded by reticular fibers, which form the endomysium. Nerve fibers and an extensive network of continuous capillaries are also present in the endomysium. Each fascicle is surrounded by dense irregular connective tissue, termed the perimysium. Supplying blood vessels and nerves plus muscle stretch receptors (muscle spindles) are located in the perimysium. Most muscles are surrounded on the outer surface by a dense irregular connective tissue layer, the epimysium. The connective tissues of skeletal muscle are interconnected and provide a means by which contractile forces are transmitted to other tissues.

Fine Structure

Contractile myofilaments of skeletal muscle cells are primarily actin or myosin-II. In addition, the myofilaments contain other proteins involved in either binding the primary filaments together (e.g., actinins, M-line proteins) or regulating the actin and myosin-II interaction (e.g., tropomyosin, troponin).

Thin myofilaments of skeletal muscle are composed of actin, troponin, and tropomyosin (Fig. 5-8). Globular molecules (G-actin) within the myoblast polymerize to form filamentous strands (F-actin). Each globular molecule has a binding site for myosin-II. Two filamentous strands twist together to form a double helix. Filamentous tropomyosin molecules lie in the groove between the two twisted strands of F-actin. The tropomyosin covers the myosin-II binding sites on the actin. In addition, triple globular units of troponin are spaced at regular intervals along the tropomyosin. The globular subunits include TnT, which binds troponin to tropomyosin; TnC, which binds calcium; and TnI, which binds to actin and prevents interaction with myosin. When calcium increases and binds to TnC, tropomyosin moves off the actin-binding site and allows myosin-II to interact with actin.

Thick myofilaments are composed of myosin-II, formed by two heavy chains and four light chains of amino acids. The two heavy chains twist together to form a rodlike tail with two protruding globular heads. Two light chains are associated with each head. The heads have binding sites for actin and for adenosine triphosphate (ATP). In addition, they have adenosine triphosphatase (ATPase) activity. Individual thick filaments are bound by bands of C protein, which stabilize the filament.

The myofilaments are arranged to form the light and dark banding pattern visible in a longitudinal section of the myofibril (Fig. 5-9). Adjacent thick myofilaments and overlapping thin myofilaments form the A band. Thin myofilaments do not extend to the center of the A band, leaving a more lucent region known as the H band. The thick myofilaments are interconnected down the center of the H band by an M line. The M line contains myomesin, which links the M line to desmin, and creatine phosphokinase, which helps maintain levels of ATP for contraction. The pseudo-H zone is present on either side of the M line. In this region, thick myofilaments lack protruding cross-bridges and the area appears more electron-lucent.

FIGURE 5-7 The myofibers are organized into fascicles (bundles) and separated from other fascicles by perimysium. Within the larger divisions of the perimysium, notice the arteriole (A), venule (V), intramuscular nerve branch (N), and muscle spindle (*). At the margin of the section is a portion of the epimysium (arrowheads) (×125)

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