Smooth muscle cells have structures called caveolae, which increase the surface-to-volume ratio of the cells. These caveolae are closely positioned near the underlying sarcoplasmic reticulum (SR). There is a gap of approximately 15 nm between the caveolae and the underlying SR, similar to the gap between T tubules and terminal SR in skeletal muscle. The presence of "Ca++ sparks" and various Ca++-handling proteins near the caveolae suggests that they may contribute to the regulation of intracellular calcium levels in smooth muscle. Caveolae are associated with the voltage-gated L-type calcium channel and the 3Na+-1Ca++ antiporter. Caveolin and cholesterol are critical for the formation of caveolae, and it is believed that caveolae may contain other signaling molecules in addition to calcium signaling.

Smooth muscle also possesses an intracellular membrane network of SR, which serves as a reservoir for calcium. When stimulatory neurotransmitters, hormones, or drugs bind to receptors on the sarcolemma, calcium can be released from the SR into the myoplasm. The SR of smooth muscle contains intracellular calcium channels, including the ryanodine receptor (RYR) and the inositol 1,4,5-trisphosphate (InsP3)-gated calcium channel. Activation of the RYR is typically triggered by an increase in intracellular calcium concentration, while the InsP3-gated calcium channel is activated by InsP3 produced upon hormone binding. Intracellular calcium concentration is lowered by the action of an SR calcium ATPase (SERCA) and extrusion of calcium from the cell through a 3Na+-1Ca++ antiporter and a sarcolemmal calcium ATPase. The amount of SR in smooth muscle cells varies from 2% to 6% of cell volume, similar to that of skeletal muscle. Chemical signals such as InsP3 or localized increases in intracellular calcium concentration functionally connect the sarcolemma and the SR.

Smooth muscle cells contain a prominent rough endoplasmic reticulum and Golgi apparatus, located centrally at each end of the nucleus. These structures play important roles in protein synthesis and secretion. The scattered mitochondria in smooth muscle cells are sufficient for oxidative phosphorylation, which generates the ATP required for contraction.

Unlike skeletal muscle, smooth muscle lacks the transverse alignment of thick and thin filaments that result in striations. Instead, the thick and thin filaments in smooth muscle are tightly packed and not uniformly aligned, giving smooth muscle its characteristic absence of striations. However, the thick and thin filaments are organized in contractile units that resemble sarcomeres.
Fig. 14.3B–D ). Caveolae increase the surface-to-volume ratio of the cells and are often closely apposed to the underlying SR. A gap of approximately 15 nm has been observed between the caveolae and the underlying SR, comparable to the gap between the T tubules and terminal SR in skeletal muscle. Moreover, “Ca++ sparks” and a variety of Ca++-handling proteins have been observed in the vicinity of caveolae, thus raising the possibility that the caveolae and the underlying SR may contribute to regulation of intracellular [Ca++] in smooth muscle. The voltage-gated L-type Ca++ channel and the 3Na+-1Ca++ antiporter, for example, are associated with caveolae. The proteins caveolin and cholesterol are both critical for the formation of caveolae, and it is hypothesized that the caveolae reflect a specialized region of the sarcolemma that may also contain various signaling molecules in addition to the Ca++ signaling mentioned earlier.
Smooth muscle also has an intracellular membrane network of SR that serves as an intracellular reservoir for Ca++ (see
Fig. 14.3B–D ). Calcium can be released from the SR into the myoplasm when stimulatory neurotransmitters, hormones, or drugs bind to receptors on the sarcolemma. Importantly, intracellular Ca++ channels in the SR of smooth muscle include the ryanodine receptor (RYR), which is similar to that found in skeletal muscle SR, and the inositol 1,4,5-trisphosphate (InsP3)-gated Ca++ channel. The RYR is typically activated by a rise in intracellular [Ca++] (i.e., Ca++-induced release of Ca++ in response to an influx of Ca++ through the sarcolemma). The InsP3-gated Ca++ channel is activated by InsP3, which is produced when a hormone or hormones bind to various Ca++-mobilizing receptors on the sarcolemma. Intracellular [Ca++] is lowered through the action of an SR Ca++-ATPase (SERCA) and extrusion of Ca++ from the cell via a 3Na+-1Ca++ antiporter and a sarcolemmal Ca++-ATPase. The amount of SR in smooth muscle cells varies from 2% to 6% of cell volume and approximates that of skeletal muscle. Chemical signals such as InsP3 or a localized increase in intracellular [Ca++] (e.g., within the gap between the caveolae and SR) functionally link the sarcolemma and the SR.
Smooth muscle cells contain a prominent rough endoplasmic reticulum and Golgi apparatus, which are located centrally at each end of the nucleus. These structures reflect significant protein synthetic and secretory functions. The scattered mitochondria are sufficient for oxidative phosphorylation to generate the increased adenosine triphosphate (ATP) consumed during contraction.
The thick and thin filaments of smooth muscle cells are about 10,000 times longer than their diameter and are tightly packed. Therefore the probability of observing an intact filament by electron microscopy is extremely low. In contrast to skeletal muscle, which contains a transverse alignment of thick and thin filaments that results in striations, the contractile filaments in smooth muscle are not in uniform transverse alignment, and thus smooth muscle has no striations. The lack of striations in smooth muscle does not imply a lack of order. The thick and thin filaments are organized in contractile units that are analogous to sarcomeres.