Basal electrical rhythm
The basal or basic electrical rhythm (BER) or electrical control activity (ECA) is the spontaneous depolarization and repolarization of pacemaker cells known as interstitial cells of Cajal (ICCs) in the smooth muscle of the stomach, small intestine, and large intestine. This electrical rhythm is spread through gap junctions in the smooth muscle of the GI tract.[1] These pacemaker cells, also called the ICCs, control the frequency of contractions in the gastrointestinal tract. The cells can be located in either the circular or longitudinal layer of the smooth muscle in the GI tract; circular for the small and large intestine, longitudinal for the stomach.[2] The frequency of contraction differs at each location in the GI tract beginning with 3 per minute in the stomach, then 12 per minute in the duodenum, 9 per minute in the ileum, and a normally low one contraction per 30 minutes in the large intestines that increases 3 to 4 times a day due to a phenomenon called mass movement.[2] The basal electrical rhythm controls the frequency of contraction but additional neuronal and hormonal controls regulate the strength of each contraction.
Physiology
The physical contractions of the smooth muscle cells can be caused by
The
The specific mechanism for the contraction of smooth muscle in the GI tract depends upon
Frequency
The number of action potentials during the plateau of a particular BER slow wave can vary. This variation in action potential generation does not impact the frequency of waves through the GI tract, only the strength of those contractile waves.[2]
Factors that impact gastric motility
- Gastrin - Stimulates increased contraction force and motility in the stomach, small intestine, and large intestine.[2]
- CCK - Suppresses motility in the stomach and duodenum[5] Additionally, CCK stimulates secretion of PPY and inhibits the secretion of ghrelin.[5]
- PPY - inhibition of upper GI tract motility
- GLP-1 - Functions as an "Ileal Brake" to inhibit upper GI tract motility when the distal gut is exposed to unabsorbed nutrients.[5] Slows gastric emptying to promote nutrient absorption.[5]
- Distension of the stomach increases motility of the stomach.[2]
- Distension of the duodenum inhibits stomach motility in order to prevent the over filling of the duodenum.[2]
- Presence of fat, low pH, and hypertonic solutions cause a decrease in motility of the stomach.[2]
- Sympathetic nervous system innervation inhibits gastric motility.[2]
- Parasympathetic nervous system innervation stimulates gastric motility.[2]
- Rate and motility are also dependent upon the meal composition. Meals that are solid and contain a greater macronutrient composition require slower and more forceful contraction in order to extract the maximum amount of nutrients throughout the GI tract.[5]
The cells that respond to and secrete these substances include I cells and K cells in the proximal small intestine, whose stimulation is dependent on nutrient exposure and entry into the duodenum, and L cells in the distal small intestine and colon which are stimulated by unabsorbed nutrients and gastric emptying.[5]
The frequency of the BER, and thus the contractions, changes throughout the GI tract. The frequency in the stomach is 3 per minute, while the duodenum is 11 to 12 per minute and the ileum is 9 per minute.[1] The colon can have a BER frequency between 2 and 13 per minute. The electrical activity is oscillatory, so that the BER has peaks and valleys when graphed over time.
See also
- Neurogastroenterology
References
- ^ a b c d e f Wood, Jackie D. (2009), "Gastrointestinal Physiology", in Rhoades, Rodney A.; Bell, David R. (eds.), Medical Physiology: Principles for Clinical Medicine (3 ed.), Philadelphia, PA: Lippincott Williams & Wilkins, pp. 463–496
- ^ a b c d e f g h i j Widmaier, Eric P., Hershel Raff, and Kevin T. Strang. Vander's Human Physiology: The Mechanisms of Body Function. New York, NY: McGraw-Hill Education, 2016.
- PMID 9662380.
- ^ a b c Ju, Yue-Kun, Elizabeth A. Woodcock, David G. Allen, and Mark B. Cannell. "Inositol 1,4,5-trisphosphate Receptors and Pacemaker Rhythms." Journal of Molecular and Cellular Cardiology 53.3 (2012): 375-81.
- ^ a b c d e f Wu T, Rayner C, Young R, Horowitz M. Gut motility and enteroendocrine secretion. Current Opinion In Pharmacology [serial online]. December 1, 2013;13(Gastrointestinal * Endocrine and metabolic diseases):928-934. Available from: ScienceDirect, Ipswich, MA.