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9.1 Smooth Muscle Contractile Process

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9.1 Smooth Muscle Contractile Process 9.1 Smooth Muscle Contractile Process The three muscle types all have a specialized contractile apparatus made up of thin actin filaments that slide relative to stationary thick myosin filaments in response to a rise in cytosolic Ca+2 to accomplish contraction. Also, they all directly use ATP as the energy source for cross-bridge cycling. Both smooth and skeletal muscle cells are elongated, but in contrast to their large, cylindrical skeletal muscle counterparts, smooth muscle cells are spindle shaped, have a single nucleus, and are considerably smaller. Also unlike skeletal muscle cells, a single smooth muscle cell does not extend the full length of a muscle. Instead, groups of smooth muscle cells are typically arranged in sheets. A smooth muscle cell has three types of filaments: (1) thick myosin filaments, which are longer than those in skeletal muscle; (2) thin actin filaments, which contain tropomyosin but lack troponin; and (3) filaments of intermediate size, which do not directly participate in contraction but are part of the cytoskeletal framework that supports the cell shape. Smooth muscle filaments are not arranged in the sarcomere pattern found in skeletal muscle. Thus, smooth muscle cells do not show the banding or striation of skeletal muscle (hence the term smooth). Lacking sarcomeres, smooth muscle does not have Z lines, but it does have dense bodies containing the same protein constituent found in Z lines. Dense bodies are positioned throughout the smooth muscle cell, as well as attached to the internal surface of the plasma membrane. Dense bodies are held in place by a scaffold of intermediate filaments. Considerably more actin is present in smooth muscle cells than in skeletal muscle cells. Unlike in skeletal muscle, myosin molecules are arranged in a smooth-muscle thick filament so that cross bridges are present along the entire filament length (that is, there is no bare portion in the center of a smooth-muscle thick filament). As a result, the surrounding thin filaments can be pulled along the thick filaments for longer distances than in skeletal muscle. Also dissimilar to skeletal muscle (in which all thin filaments surrounding a thick filament are pulled toward the center of the stationary thick filament), the myosin proteins in smooth muscle thick filaments are organized so that half of the surrounding thin filaments are pulled toward one end of the stationary thick filament and the other half are pulled toward the opposite end. The thin filaments of smooth muscle cells do not contain troponin, and tropomyosin does not block actin’s cross-bridge binding sites. Light-weight chains of proteins are attached to the heads of myosin molecules. These so called light chains are only of secondary importance in skeletal muscle, but they have a crucial regulatory function in smooth muscle. Smooth muscle myosin can interact with actin only when the light chain is phosphorylated. 82 Ch 9: Comparative Physiology of Skeletal, Smooth, and Cardiac Fibers During excitation, the increased cytosolic Ca+2 acts as an intracellular messenger, initiating a chain of biochemical events that results in phosphorylation of the myosin light chain. Smooth muscle Ca+2 binds with calmodulin, an intracellular protein found in most cells that is structurally similar to troponin. This Ca+2–calmodulin complex binds to and activates another protein, myosin light chain kinase (MLC kinase), which in turn phosphorylates the myosin light chain. This phosphate on the myosin light chain is in addition to the phosphate accompanying ADP on the myosin cross-bridge ATPase site during the energy-supplying cycle that powers cross-bridge bending. The Pi on the light chain permits the myosin cross bridge to bind with actin so that cross-bridge cycling can begin. Therefore, smooth muscle is triggered to contract by a rise in cytosolic Ca+2, similar to what happens in skeletal muscle, but in smooth muscle, Ca+2 ultimately turns on the cross bridges by inducing a chemical change in myosin in the thick filaments (phosphorylation), whereas in skeletal muscle it exerts its effects by causing a physical change at the thin filaments (moving troponin and tropomyosin from their blocking positions). Tonic and Phasic Smooth Muscle Smooth muscle can be grouped into two categories: phasic smooth muscle and tonic smooth muscle. Phasic smooth muscle contracts in bursts, triggered by action potentials that lead to increased cytosolic Ca+2. It is most abundant in the walls of hollow organs that push contents through them, such as digestive organs. Tonic smooth muscle is usually partially contracted at all times; that is, it exhibits smooth muscle tone. Tone exists because this type of smooth muscle has a low resting potential of -55 to -40 mV. Some surface membrane voltage-gated Ca+2 channels are open at these potentials. The resultant Ca+2 entry maintains a state of partial contraction, or tone, in the absence of action potentials. Tonic smooth muscle does not display bursts of contractile activity but instead changes its extent of contraction above or below this tonic level in response to regulatory factors, which alter the cytosolic Ca+2 concentration. Because a smooth muscle cell has no T tubules and a poorly developed SR, in phasic smooth muscle, the increased cytosolic Ca+2 that triggers contraction comes from two sources: most Ca+2 (1) enters from the extracellular fluid (ECF), but some is (2) released intracellularly from the sparse SR stores. Unlike their role in skeletal muscle cells, voltage-sensitive dihydropyridine receptors in the plasma membrane of smooth muscle cells function as Ca+2 channels. When these surface-membrane channels are opened in response to an action potential, Ca+2 enters down its concentration gradient from the ECF. The entering Ca+2 triggers the opening of Ca+2 channels in the SR so that small additional amounts of Ca+2 are released intracellularly from this meager source. One of the major means of increasing contractile activity in tonic smooth muscle is binding of an extracellular chemical messenger, such as norepinephrine or various hormones, to a G-protein-coupled receptor, which activates the IP3–Ca+2 second-messenger pathway. The membrane of the SR in tonic smooth muscle has IP3 receptors, which like ryanodine receptors, are Ca+2 -release channels. IP3 binding leads to release of contractile-inducing Ca+2 from this intracellular store into the cytosol. This is how norepinephrine released from the sympathetic nerve endings acts on arterioles to increase blood pressure. Relaxation in smooth muscle is accomplished by removal of Ca+2 as it is actively transported out across the plasma membrane or back into the SR, depending on its source. When Ca+2 is removed, myosin is dephosphorylated (the phosphate is removed) and can no longer interact with actin, so the muscle relaxes. Ch 9: Comparative Physiology of Skeletal, Smooth, and Cardiac Fibers 83 Multi-Unit and Single-Unit Smooth Muscle Smooth muscle is grouped into two categories—multi-unit and single-unit smooth muscle. A multiunit smooth muscle consists of multiple discrete units that function independently of one another and must be separately stimulated by nerves to undergo action potentials and contract (similar to skeletal muscle motor units). Thus, its contractile activity is neurogenic. Unsurprisingly, all multiunit smooth muscle is phasic, contracting only when neutrally stimulated (autonomic innervation). Multiunit smooth muscle is found (1) in the walls of large blood vessels; (2) in small airways to the lungs; (3) in the muscle of the eye that adjusts the lens for near or far vision; (4) in the iris of the eye, which alters the pupil size; and (5) at the base of hair follicles. Single-Unit Smooth Muscle Most smooth muscle is single-unit smooth muscle, alternatively called visceral smooth muscle, because it is found in the walls of the hollow organs or viscera (for example, the digestive, reproductive, and urinary tracts and small blood vessels). The muscle fibers that make up this type of muscle become excited and contract as a single unit. This’s possible because these fibers are electrically linked by gap junctions. When an action potential occurs anywhere within a sheet of single-unit smooth muscle, it is quickly propagated via these junctions throughout the entire group of cells, which then contract as a single, coordinated unit. Such a group of interconnected muscle cells that function electrically and mechanically as a unit is known as a functional syncytium. Single-unit smooth muscle is self-excitable, so it does not require nervous stimulation for contraction. Single-unit smooth muscle may be of the phasic or tonic type. Specialized cells within a single-unit muscle display spontaneous electrical activity; that is, they can undergo action potentials without any external stimulation. These specialized self-excitable cells do not maintain a constant resting potential. Instead, their membrane potential inherently fluctuates without any factors external to the cell. Two major types of spontaneous depolarizations displayed by self-excitable cells are pacemaker potentials and slow-wave potentials. With pacemaker potentials, the membrane potential gradually depolarizes on its own because of shifts in passive ionic fluxes accompanying automatic changes in ion channel permeability. When the membrane has depolarized to threshold, an action potential is initiated. After repolarizing, the membrane potential again depolarizes to threshold, cyclically continuing in this manner to repetitively self- generate action potentials. Only a few of all the cells in a functional syncytium (or a single-unit smooth muscle) are non-contractile, pacemaker (or self-excitable) cells. Most smooth muscle cells are specialized to contract but cannot self- initiate action potentials. However, once an action potential is initiated by a self-excitable pacemaker cell, it is conducted to the remaining contractile, non-pacemaker cells of the syncytium via gap junctions, so the entire group of connected cells contracts as a unit without any nervous input.
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