9.8 Structure of Smooth Muscle
- Each smooth muscle cell is spindle-shaped, they are much smaller than skeletal muscle fibers.
- Many individual smooth muscle cells are generally interconnected to form sheetlike layers of cells.
- Skeletal muscle fibers are multinucleate cells with limited ability to divide once they have differentiated; smooth muscle cells have a single nucleus and have the capacity to divide throughout the life of an individual.
- A variety of paracrine factors can stimulate smooth muscle cells to divide, often in response to tissue injury.
- Just like skeletal muscle fibers, smooth muscle cells have thick myosin-containing filaments and thin actin-containing filaments.
- A protein called caldesmon also associates with the thin filaments; in some types of muscle, it may function in regulating contraction.
- The thin filaments are anchored either to the plasma membrane or to cytoplasmic structures known as dense bodies, which are functionally similar to the Z lines in skeletal muscle fibers.
- Note in Figure 9.33 that the filaments are oriented diagonally to the long axis of the cell. When the fiber shortens, the regions of the plasma membrane between the points where actin is attached to the membrane balloon out.
- Nevertheless, smooth muscle contraction occurs by a sliding-filament mechanism.
- In smooth muscle, significant force is generated over a relatively broad range of muscle lengths compared to that of skeletal muscle.
- This property is highly adaptive because most smooth muscles surround hollow structures and organs that undergo changes in volume with accompanying changes in the lengths of the smooth muscle fibers in their walls.
- Even with relatively large increases in volume, as during the accumulation of large amounts of urine in the bladder, the smooth muscle fibers in the wall retain some ability to develop tension, whereas such distortion might stretch skeletal muscle fibers beyond the point of thick and thin filament overlap.
9.9 Smooth Muscle Contraction and Its Control
Changes in cytosolic Ca2+ concentration control the contractile activity in smooth muscle fibers, as in striated muscle.
- Because smooth muscle lacks the Ca2+-binding protein troponin, tropomyosin is never held in a position that blocks cross-bridge access to actin.
- Thus, the thin filament is not the main switch that regulates cross-bridge cycling.
- Instead, cross-bridge cycling in smooth muscle is controlled by a Ca2+-regulated enzyme that phosphorylates myosin.
- Only the phosphorylated form of smooth muscle myosin can bind to actin and undergo crossbridge cycling.
- Figure 9.34 Activation of smooth muscle contraction by Ca2+. See text for description of the numbered steps.
- Many inputs to a smooth muscle plasma membrane can alter the contractile activity of the muscle (Table 9.5).
- This contrasts with skeletal muscle, in which membrane activation depends only upon synaptic inputs from somatic neurons.
- Some inputs to smooth muscle increase contraction, and others inhibit it. Moreover, at any one time, the smooth muscle plasma membrane may
- be receiving multiple inputs, with the contractile state of the muscle dependent on the relative intensity of the various inhibitory and excitatory stimuli.
- All these inputs influence contractile activity by altering cytosolic Ca2+ concentration as described in the previous section.
- Some smooth muscles contract in response to membrane depolarization, whereas others can contract in the absence of any membrane potential change.
- Interestingly, in smooth muscles in which action potentials occur, calcium ions, rather than sodium ions, carry a positive charge into the cell during the rising phase of the action potential—that is, depolarization of the membrane
- opens voltage-gated Ca2+ channels, producing Ca2+-mediated rather than Na+-mediated action potentials.
- Smooth muscle is different from skeletal muscle in another important way with regard to electrical activity and cytosolic Ca2+ concentration.
- Smooth muscle cytosolic Ca2+ concentration can be increased (or decreased) by graded depolarizations (or hyperpolarizations) in membrane potential, which increase or decrease the number of open Ca2+ channels.
Membrane activation: Nerves and Hormones
- The contractile activity of smooth muscles is influenced by neurotransmitters released by autonomic neuron endings.
- Unlike skeletal muscle fibers, smooth muscle cells do not have a specialized motor end-plate region.
- As the axon of a postganglionic autonomic neuron enters the region of smooth muscle cells, it divides into many branches, each branch containing a series of swollen regions known as varicosities.Each varicosity contains many vesicles filled with neurotransmitter, some of which are released when an action potential passes the varicosity.
- Therefore, a number of smooth muscle cells are influenced by the neurotransmitters released by a single neuron, and a single smooth muscle cell may be influenced by neurotransmitters from more than one neuron.
- Whereas some neurotransmitters enhance contractile activity, others decrease contractile activity. This is different than in skeletal muscle, which receives only excitatory input from its motor neurons; smooth muscle tension can be either increased or decreased by neural activity.
- Moreover, a given chemical signal may produce opposite effects in different smooth muscle tissues.
- In addition to receptors for neurotransmitters, smooth muscle plasma membranes contain receptors for a variety of hormones.
- Binding of a hormone to its receptor may lead to either increased or decreased contractile activity.
Membrane activation: local factors
- Local factors, including paracrine signals, acidity, oxygen and carbon dioxide concentration, osmolarity, and the ionic composition of the extracellular fluid, can also alter smooth muscle tension.
- Responses to local factors provide a means for altering smooth muscle contraction in response to changes in the muscle’s immediate internal environment, which can lead to regulation that is independent of long-distance signals from nerves and hormones.
- Many of these local factors induce smooth muscle relaxation.
- Nitric oxide (NO) is one of the most commonly encountered paracrine compounds that produce smooth muscle relaxation.
- NO is released from some axon terminals as well as from a variety of epithelial and endothelial (blood vessel) cells. Because of the short life span of this reactive molecule, it influences only those cells that are very near its release site.
- Some smooth muscles can also respond by contracting when they are stretched. Stretching opens mechanically gated ion channels, leading to membrane depolarization. The resulting contraction opposes the forces acting to stretch the muscle.
- At any given moment, smooth muscle cells in the body receive many simultaneous signals. The state of contractile activity that results depends on the net magnitude of the signals promoting contraction versus those promoting relaxation.
- This is a classic example of the general principle of physiology that most physiological functions are controlled by multiple regulatory systems, often working in opposition
15.2 Structure of the Gastrointestinal Tract Wall- epithelium
- From the mid-esophagus to the anus, the wall of the GI tract has the general structure illustrated in Figure 15.5.
- In some regions, the apical (luminal) surface is highly convoluted, a feature that greatly increases the surface area available for absorption.
- From the stomach on, this surface is covered by a single layer of epithelial cells linked together along the edges of their apical surfaces by tight junctions (see Figure 3.9b).
- Invaginations of the epithelium into the underlying tissue form exocrine glands that secrete acid, HCO 3− enzymes, water, ions, and mucus into the lumen.
- Other cells in the epithelium secrete hormones into the blood that are important in regulating various aspects of digestion and appetite.
15.2 Structure of the Gastrointestinal Tract Wall: lamina propria
- Surrounding the epithelium is the lamina propria, which is a layer of loose connective tissue through which pass small blood vessels, neurons, and lymphatic vessels. (Some of these structures do not appear in Figure 15.5 but are shown in detail in Figure 15.18.)
15.2: muscularis mucosa
- The lamina propria is separated from underlying tissues by the muscularis mucosa, which is a thin layer of smooth muscle involved in small movements of the mucosal surface.
- The combination of these three layers—the epithelium, lamina propria, and muscularis mucosa—is called the mucosa (see Figure 15.5).
- Outside of the mucosa is the submucosa, which is a second connective-tissue layer.
- This layer also contains blood and lymphatic vessels, and a network of neurons, the submucosal plexus.
- Neurons project from this network to epithelial cells in the apical surface.
15.2: muscularis externa
- Surrounding the submucosa are layers of smooth muscle called the muscularis externa.
- Contractions of these muscles provide the forces for moving and mixing the gastrointestinal contents.
- Except in the stomach, which has three layers, elsewhere the muscularis externa has two layers:
- (1) a relatively thick inner layer of muscle, the fibers of which are oriented in a circular pattern around the tube so that contraction produces a narrowing of the lumen; and
- (2) a thinner outer layer of longitudinal muscle, the contraction of which shortens the tube.
- Also includes myecentric plexus
15.2 myenteric plexus
- Between these two muscle layers is a second network of neurons known as the myenteric plexus.
- Neurons interconnect this network with the submucous plexus, and also project into the surrounding smooth muscle layers.
- The myenteric plexus is innervated by nerves from the sympathetic and parasympathetic divisions of the autonomic nervous system.
- This complex, local neural network is described in detail later in this chapter.
- Finally, the outer surface of the tube is a thin layer of connective tissue called the serosa.
- Thin sheets of connective tissue connect the serosa to the abdominal wall and support the GI tract in the abdominal cavity.
Cell replacement and division
- Epithelial surfaces in the GI tract are continuously being replaced by new epithelial cells.
- In the small intestine, for example, new cells arise by cell division from cells at the base of the fingerlike villi that project into the lumen.
- These cells differentiate as they migrate to the top of the villi, replacing older cells that die and are discharged into the intestinal lumen.
- These dead cells release their intracellular enzymes into the lumen, which then contribute to the digestive process.
- About 17 billion epithelial cells are replaced each day, and the entire epithelium of the small intestine is replaced approximately every 5 days.
- It is because of this rapid cell turnover that the lining of the intestinal tract is so susceptible to damage by treatments that inhibit cell division, such as anticancer drugs and radiation therapy.
- Also at the base of the villi are enteroendocrine cells that secrete hormones that, as you will learn, control a wide variety of gastrointestinal functions, including motility and exocrine pancreatic secretions.