Functional Aspects of Smooth Muscle
Smooth muscle is specialized for slow, prolonged contraction.
As noted previously, smooth muscle cells may enter the latch state and remain contracted for long periods of time without fatiguing. They may contract in a wavelike manner, producing peristaltic movements such as those in the gastrointestinal tract and the male genital tract, or contraction may occur along the entire muscle, producing extrusive movements (e.g., those in the urinary bladder, gallbladder, and uterus). Smooth muscle exhibits a spontaneous contractile activity in the absence of nerve stimuli.
Contraction of smooth muscle is usually regulated by post-synaptic neurons of the autonomic nervous system (ANS); most smooth muscle is directly innervated by both sympathetic and parasympathetic nerves. In the gastrointestinal tract, the third component of the ANS, the enteric division, is the primary source of nerves to the muscular layers.
FIGURE 11.23 • Schematic diagram illustrating steps leading to initiation of smooth muscle contraction. An increase in the Ca2 level concentration within the cytosol is necessary to initiate smooth muscle contraction. This increase is achieved either by initial depolarization of the cell membrane or hormonal stimulation of cell surface receptors. The intracellular Ca2 binds to calmodulin (4 Ca2 per 1 molecule of calmodulin) to form the Ca2–calmodulin complex. This complex then binds to myosin light chain kinase (MLCK) to phosphorylate one of the two regulatory light chains of the myosin molecule. When phosphorylated, the myosin changes its conformation and the actin-binding site on the myosin head is activated, allowing it to attach to actin. In the presence of ATP, the myosin head bends, producing contraction. sER, smooth endoplasmic reticulum.
Although Ca2 enters the cytoplasm during depolarization by voltage-gated Ca2 channels, some Ca2 channels, called ligand-gated Ca2 channels, are activated by hormones via their second-messenger pathways (see Fig. 11.23). Thus, smooth muscle contraction may also be initiated by certain hormones secreted from the posterior pituitary gland (e.g., oxytocin and, to a lesser extent, antidiuretic hormone [ADH]). In addition, smooth muscle cells may be stimulated or inhibited by hormones secreted by the adrenal medulla (e.g., epinephrine and norepinephrine). Also oxytocin is a potent stimulator of smooth muscle contraction, and its release by the posterior pituitary plays an essential role in uterine contraction during parturition. It is often used to induce or enhance labor. Many peptide secretions of enteroendocrine cells also stimulate or inhibit smooth muscle contraction, particularly in the alimentary canal and its associated organs.
Nerve terminals in smooth muscle are observed only in the connective tissue adjacent to the muscle cells.
Nerve fibers pass through the connective tissue within the bundles of smooth muscle cells; enlargements in the passing nerve fiber, or bouton en passant (see page 359), occur adjacent to the muscle cells to be innervated. The enlargements contain synaptic vesicles with neuromuscular transmitters. However, the neuromuscular site is not comparable to the neuromuscular junction of striated muscle. Rather, a considerable distance, usually 10 to 20 m (in some locations, up to 200 m), may separate the nerve terminal and the smooth muscle. The neurotransmitter released by the nerve terminal must diffuse across this distance to reach the muscle.