The gastric mucosal barrier protects the surface of the stomach (Fig. 29.11). It consists of a 0.2 mm thick mucus gel layer that effectively separates the HCO3 −-rich secretions of the surface epithelial cells from the acidic contents of the gastric lumen. This mucus layer helps maintain a nearly neutral pH at the surface of the epithelial cells, despite the low luminal pH of about 2. Additionally, the mucus layer slows down the diffusion of acid and pepsins towards the epithelial cell surface. Thus, the protection of the gastric epithelium relies on both mucus and HCO3 − secretion.

To comprehend gastrointestinal (GI) motility, it is essential to understand some aspects of smooth muscle function. The motion of the gut wall determines the movement of luminal contents along its length. The primary patterns of motility are mixing (segmentation) and propulsion (peristalsis). Moreover, smooth muscle activity in the stomach and colon serves a storage function.

The smooth muscle found in the GI tract shares structural similarities with other smooth muscle in the body. Bundles of fusiform cells are tightly packed together and surrounded by a connective tissue sheath. Functionally, the smooth muscle cells are coupled via gap junctions, allowing bundles to contract synchronously. In the intestinal wall, there exist specialized cells called interstitial cells of Cajal (ICCs) (Fig. 29.12). These cells play a role in transmitting information from enteric neurons to smooth muscle cells. It is believed that ICCs also act as "pacemaker" cells, generating the basic electrical rhythm known as slow-wave activity, which is a consistent feature of GI smooth muscle (Fig. 29.13).

The electrophysiology of GI smooth muscle involves cyclic variations in the resting membrane potential known as slow waves. In the stomach, the frequency of slow waves is 3 to 5 per minute, while in the small intestine, it is approximately 12 to 20 per minute. In the colon, the frequency decreases to 6 to 8 per minute. The pacemaker region in different parts of the GI tract determines the frequency of slow waves, and it is believed that ICCs are responsible for generating these waves. ICCs are located in a thin layer between the longitudinal and circular layers of the muscularis externa, as well as in other areas of the GI tract wall. These cells have properties of both fibroblasts and smooth muscle cells. Their elongated processes form gap junctions with the longitudinal and circular smooth muscle cells, enabling rapid conduction of the slow waves to both muscle layers. Gap junctions electrically and chemically couple the smooth muscle cells of both layers, allowing the slow wave to spread throughout the smooth muscle in each segment of the GI tract (Fig. 29.12).

The strength of muscle contraction is determined by the amplitude of the slow wave (Fig. 29.13). When the slow wave reaches a threshold amplitude, it initiates a contraction in the smooth muscle. The release of neurotransmitters from enteric neurons can alter the amplitude of the slow wave. At rest, the membrane potential and muscle tone are unaffected. However, stimulation of enteric neurons increases the membrane potential and muscle tone, while inhibition of enteric neurons decreases the membrane potential and muscle tone.
Fig. 29.11 ). The mucus gel layer, which is about 0.2 mm thick, effectively separates the HCO3 −-rich secretions of the surface epithelial cells from the acidic contents of the gastric lumen. The mucus allows the pH of epithelial cells to be maintained at nearly neutral despite a luminal pH of about 2. Mucus also slows the diffusion of acid and pepsins to the epithelial cell surface. Protection of the gastric epithelium depends on both mucus and HCO3 − secretion.
To understand GI motility it is necessary to review some properties of smooth muscle function. The motion of the gut wall governs the flow of the luminal contents along its length; the main patterns of motility are mixing (segmentation) and propulsion (peristalsis). In addition, smooth muscle activity in the stomach and colon subserves a storage function.
• Fig.29.11The surface of the stomach is protected by the gastric mucosal barrier. Buffering by the HCO3 −-rich secretions and the high viscosity of the layer of mucus allow the pH at the cell surface to remain near 7, whereas the pH in the gastric juice in the lumen is 2.
Functional Anatomy of Gastrointestinal Smooth Muscle
The smooth muscle in the GI tract is similar in structure to other smooth muscle found in the body. Fusiform cells are packed together in bundles surrounded by a connective tissue sheath. Gap junctions functionally couple the smooth muscle cells so that contraction of bundles occurs synchronously. The interstitial cells of Cajal (ICCs) are a specialized group of cells in the intestinal wall that are involved in transmission of information from enteric neurons to smooth muscle cells (
Fig. 29.12 ). It is also thought that ICCs are “pacemaker” cells that have the capacity to generate the basic electrical rhythm, or slow-wave activity, that is a consistent feature of GI smooth muscle (
Fig. 29.13).
Electrophysiology of Gastrointestinal Smooth Muscle
The cyclic variation in resting membrane potential of GI smooth muscle is called the basic electrical rhythm or slow wave. The frequency of slow waves is 3 to 5 per minute in the stomach and about 12 to 20 per minute in the small intestine; it decreases to 6 to 8 per minute in the colon. The frequency of the slow wave is set by a pacemaker region in the different regions of the GI tract (see
Fig. 29.13 ). Slow waves are thought to be generated by ICCs. These cells are located in a thin layer between the longitudinal and
Slow waves are generated in interstitial cells of Cajal
Slow wave conducted to smooth muscle cells • Fig.29.12Diagrammatic representation of the interstitial cells of Cajal network in the smooth muscle wall of the GI tract.
circular layers of the muscularis externa and in other places in the wall of the GI tract. Interstitial cells have properties of both fibroblasts and smooth muscle cells. Their long processes form gap junctions with the longitudinal and circular smooth muscle cells; the gap junctions enable the slow waves to be conducted rapidly to both muscle layers. Because gap junctions electrically and chemically couple the smooth muscle cells of both longitudinal and circular layers, the slow wave spreads throughout the smooth muscle of each segment of the GI tract.
538 SECTION6Berne & Levy Physiology • Fig.29.13Amplitude of slow wave determines the strength of muscle contraction. The slow wave will initiate a contraction in smooth muscle when it reaches a threshold amplitude. The amplitude of the slow wave is altered by release of neurotransmitters from enteric neurons. At rest Stimulated Inhibited Membrane potential Muscle tone Membrane potential Muscle tone Membrane potential Muscle tone