Gastrointestinal Smooth Muscle

The smooth muscle cells in each part of the gastrointestinal (GI) tract have structural and functional differences. However, certain basic properties are common to all of these cells. Smooth muscle cells make up all of the contractile tissue of the GI tract with the exception of the pharynx, the upper one-third to one-half of the esophagus, and the external anal sphincter, which are striated muscle.

Structure of Smooth Muscle Cells

Smooth muscle cells are smaller than skeletal muscle cells and are long, narrow, and spindle shaped. Most are 4-10 mm wide and 50-200 mm long. Cells are loosely packed with relatively large intracellular spaces that contain bands of collagen, elastin, and other connective tissue. This network allows contractile forces to be transmitted from one cell to others nearby. Cells are arranged in bundles that branch and anastomose with one another. These bundles, or fasciae, are surrounded by connective tissue and are the functional units of gut smooth muscle.

The cells belonging to a bundle are functionally coupled so that contractions of all cells are synchronous. Smooth muscle tissue is therefore classified as unitary (Fig. 1). Coupling occurs by actual fusion of cell membranes to form areas of low electrical resistance termed gap junctions or nexuses. Only a few smooth muscle cells in each bundle are actually innervated. The nerve axons run through the bundles releasing neurotransmitters from swellings along their length. The swellings are actually removed from the muscle cells so that no neuro-muscular junctions exist. The neurotransmitters either excite or inhibit only a few cells in each bundle, and the effect of the transmitter on membrane potential is spread directly from one cell to another.

Contractile elements of smooth muscle cells are not arranged in the orderly fashion found in skeletal muscle cells. Sarcomeres and, thus, striations are absent. Instead, the contractile proteins (actin and myosin} are arranged in myofilaments crossing from one side of the cell to the other at oblique angles. Thin filaments consist of actin and tropomyosin, and thick filaments are made up of myosin. Smooth muscle contains much more actin and less myosin and troponin than skeletal muscle. The ratio of thin to thick filaments in smooth muscle is about 15:1, compared with 2:1 for skeletal muscle. Smooth muscle cells also contain a network of intermediate filaments that form a type of internal skeleton. The contractile filaments may anchor to this network, thus transmitting their contractile force over much of the cell.

Smooth Muscle Contraction

Depolarization of circular muscle results in the rapid conduction of the depolarization around the gut so that a ring of smooth muscle contracts. The depolarization moves more slowly longitudinally from this ring of depolarized cells. The opposite occurs when longitudinal muscle is depolarized. In this case, the depolarizing current is transmitted much more rapidly in the longitudinal direction and spreads slowly around the gut.

Nexus

Nexus

FIGURE 1 Structural characteristics of unitary, smooth muscle. Cells are coupled anatomically and electrically by areas of fusion of their cell membranes. These areas are called nexuses.

In both cases, however, the depolarization moves rapidly with the long axes of the smooth muscle cells. This pattern is produced simply because the current spreads much more rapidly through the low resistance of the cytoplasm of the cells than across the higher resistance of the cell membranes. Because smooth muscle cells are 10-20 times longer than they are wide, the resistance to current per unit distance is much less over the long axis of the cells compared with the short axis.

Depolarization results in different responses from smooth muscle cells in different portions of the GI tract. Muscles of the esophagus, the distal one-third of the stomach (antrum), and the small intestine contract and relax rapidly, in a matter of seconds. These contractions are called phasic. On the other hand, the smooth muscle of the lower esophageal sphincter, the orad stomach, the ileocecal sphincter, and the internal anal sphincter sustain contractions that may last from minutes to hours. These contractions are called tonic. The type of contraction depends on the smooth muscle cell itself and is adapted to carry out the motility function of the organ involved.

The contractile pattern of the smooth muscle in most parts of the GI tract is determined by the basic electrical rhythm of depolarizations of the resting membrane potential. These oscillations in resting membrane potential are referred to as slow waves and have different frequencies in different parts of the tract (3-12 cycles/min). The slow waves determine the pattern of spike or action potentials produced. The activity of extrinsic nerves and the presence of hormones and paracrines modulate this activity, determining the strength of the contractions and whether or not variations in membrane potentials result in action potentials and subsequent contractions. Wave frequency is extremely constant and is virtually unaffected by neural and hormonal activity. Slow waves are inherent in the smooth muscle and are influenced only by body temperature and metabolic activity. As these increase, the frequency of slow waves also increases. The origin of slow waves is in cells called the interstitial cells of Cajal. These specialized cells receive a large amount of neural input and form gap junctions with smooth muscle cells.

Contractions of smooth muscle cells depend on levels of free intracellular calcium, as do contractions of other muscle cells. The threshold for interaction of the contractile proteins occurs at approximately 10—7 M calcium, and maximal contraction occurs at about 10—5 M. Points of disagreement exist regarding the actual steps involved, but the most likely summary of events is shown in Fig. 2. Calcium first binds to calmodulin, one of the calcium-binding proteins. The complex then activates a myosin light chain kinase, which in turn splits adenosine triphosphate (ATP) to phosphorylate

FIGURE 2 Biochemical steps in the contraction of smooth muscle. Increased Ca2+ activates myosin light chain kinase, phosphorylating myosin. Myosin-P then binds to actin, resulting in contraction. As Ca2+ levels decrease, the kinase is inactivated, the phosphatase removes the phosphate from myosin-P, and relaxation occurs. (Modified from Johnson LR, ed., Gastrointestinal physiology, 6th ed. St. Louis: CV Mosby, 2001.)

Contraction

FIGURE 2 Biochemical steps in the contraction of smooth muscle. Increased Ca2+ activates myosin light chain kinase, phosphorylating myosin. Myosin-P then binds to actin, resulting in contraction. As Ca2+ levels decrease, the kinase is inactivated, the phosphatase removes the phosphate from myosin-P, and relaxation occurs. (Modified from Johnson LR, ed., Gastrointestinal physiology, 6th ed. St. Louis: CV Mosby, 2001.)

one of the components of myosin. The phosphorylated form of myosin now interacts with actin to produce a contraction. The contraction is supported by the additional release of energy from ATP. As intracellular calcium levels decrease, myosin is dephosphorylated by a specific phosphatase. The interaction between myosin and actin ceases, and relaxation occurs.

The remainder of this chapter focuses on how these contractile events are produced in each part of the GI tract and how they are modified to result in the patterns of motility specific to each region.

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