Fig. 14.6 ). In general, smooth muscle is innervated by the autonomic nervous system. The smooth muscle in arteries is innervated primarily by sympathetic fibers, whereas the smooth muscle in other tissues can have both sympathetic and parasympathetic innervation. In the GI tract, smooth muscle is innervated by nerve plexuses that make up the enteric nervous system. The smooth muscle cells of some tissues (e.g., uterus) have no innervation.
The neuromuscular junctions and neuromuscular transmission in smooth muscle are functionally comparable to that of skeletal muscle but structurally less complex. The autonomic nerves that supply smooth muscle have a series of swollen areas, or varicosities, that are spaced at intervals along the axon. These varicosities contain vesicles for the neurotransmitter (see
Fig. 14.6).
The postsynaptic membrane of smooth muscle exhibits little specialization when compared with that of skeletal muscle (see ). The synaptic cleft is typically about 80 to 120 nm wide but can be as narrow as 6 to 20 nm or even greater than 120 nm. In synapses in which a wide synaptic cleft is found, release of neurotransmitter can affect multiple smooth muscle cells. There are a large number of neurotransmitters that affect smooth muscle activity. A partial listing is provided in
Table 14.1
Regulation of Contraction
Contraction of smooth muscle requires phosphorylation of a myosin light chain. Typically this phosphorylation occurs in response to a rise in intracellular [Ca++], either after an action potential or in the presence of a hormone/agonist. As depicted in
Fig. 14.7 , a rise in intracellular [Ca++] in smooth muscle results in the binding of 4 Ca++ ions to the protein calmodulin, and then the Ca++-calmodulin complex activates MLCK, which phosphorylates the regulatory light chain of myosin. This phosphorylation step is critical for the interaction of smooth muscle myosin with actin. In addition to this phosphorylation step in smooth muscle,