FIGURE 11.21 • Comparison of myosin filaments of skeletal muscle and smooth muscle. This drawing shows the different arrangements of myosin thick filaments. a. Bipolar thick filaments are present in skeletal and cardiac muscle. They have a helical parallel–antiparallel arrangement of myosin molecules with their globular heads projecting from both ends of the filament. This filament has a “bare zone” in the middle of the filaments that does not have globular heads. b. Side-polar nonhelical thick filaments are present in smooth muscle. In these filaments, myosin molecules are staggered in parallel by two immediate neighbors and are also bound to an antiparallel partner via a short overlap at the very tip of their tails. The polarity of the myosin heads is the same along the entire length of one side of the filament and the opposite on the opposite side. There is no central “bare zone”; instead, the filament b has asymmetrically tapered bare ends.
-actinin-containing cytoplasmic densities (dense bodies) actin-myosin filaments nucleus actin filament actin tropomyosin myosin filament intermediate filament (desmin, vimentin) dense body -actinin
FIGURE 11.22 • A suggested model for smooth muscle cell contraction. Bundles of myofilaments containing thin and thick filaments, shown in dark brown, are anchored on cytoplasmic densities, shown in beige. These densities, in turn, are anchored on the sarcolemma. Cytoplasmic densities are intracellular analogs of striated muscle Z lines. They contain the actin-binding protein -actinin. Because the contractile filament bundles are oriented obliquely to the long axis of the cell, their contraction shortens the cell and produces the “corkscrew” shape of the nucleus.
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 (see Fig. 11.20).
Contraction in smooth muscles is initiated by a variety of impulses, including mechanical, electrical, and chemical stimuli.
The mechanisms that cause contraction of smooth muscle cells are very different from those of striated muscle. Smooth muscle has diverse signal transduction pathways that initiate and modulate smooth muscle contraction. They all lead to elevation of the intracellular concentration of Ca2, which is directly responsible for muscle contraction. Thus muscle contraction can be triggered by the following.
 Mechanical impulses, such as passive stretching of vascular smooth muscle, activate mechanosensitive ion channels, leading to initiation of spontaneous muscle contraction (myogenic reflex).
 Electrical depolarizations can occur, such as those during neural stimulation of smooth muscle. The release of the neurotransmitters acetylcholine and norepinephrine from their synaptic nerve endings stimulates receptors located in the neuronal plasma membrane and changes the membrane potential. This causes opening of voltage-sensitive Ca2 channels (see below).
 Chemical stimuli, such as those elicited by angiotensin II, vasopressin, or thromboxane A2, act on specific cell membrane receptors, leading to muscle contraction. These substances use second-messenger pathways that do not require the generation of an action potential and cell depolarization to trigger contraction. The most common second-messenger pathways used by smooth muscle are inositol 1,4,5-trisphosphate (IP3), G-protein-coupled, and nitric oxide (NO)-cGMP pathways.
Smooth muscle cells lack a T system.