| Generation and propagation of gastric slow waves. | |
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MedLine Citation:
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PMID: 19930430 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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1. Mechanisms underlying the generation and propagation of gastrointestinal slow wave depolarizations have long been controversial. The present review aims to collate present knowledge on this subject with specific reference to slow waves in gastric smooth muscle. 2. At present, there is strong agreement that interstitial cells of Cajal (ICC) are the pacemaker cells that generate slow waves. What has been less clear is the relative role of primary types of ICC, including the network in the myenteric plexus (ICC-MY) and the intramuscular network (ICC-IM). It is concluded that both ICC-MY and ICC-IM are likely to serve a major role in slow wave generation and propagation. 3. There has been long-standing controversy as to how slow waves 'propagate' circumferentially and down the gastrointestinal tract. Two mechanisms have been proposed, one being action potential (AP)-like conduction and the other phase wave-based 'propagation' resulting from an interaction of coupled oscillators. Studies made on single bundle gastric strips indicate that both mechanisms apply with relative dominance depending on conditions; the phase wave mechanism is dominant under circumstances of rhythmically generating slow waves and the AP-like propagation is dominant when the system is perturbed. 4. The phase wave mechanism (termed Ca(2+) phase wave) uses cyclical Ca(2+) release as the oscillator, with coupling between oscillators mediated by several factors, including: (i) store-induced depolarization; (ii) resultant electrical current flow/depolarization through the pacemaker cell network; and (iii) depolarization-induced increase in excitability of downstream Ca(2+) stores. An analogy is provided by pendulums in an array coupled together by a network of springs. These, when randomly activated, entrain to swing at the same frequency but with a relative delay along the row giving the impression of a propagating wave. 5. The AP-like mechanism (termed voltage-accelerated Ca(2+) wave) propagates sequentially like a conducting AP. However, it is different in that it depends on regenerative store Ca(2+) release and resultant depolarization rather than regenerative activation of voltage-dependent channels in the cell membrane. 6. The applicability of these mechanisms to describing propagation in large intact gastrointestinal tissues, where voltage-dependent Ca(2+) entry is also likely to be functional, is discussed. |
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Authors:
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Dirk F van Helden; Derek R Laver; John Holdsworth; Mohammad S Imtiaz |
Publication Detail:
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Type: Journal Article; Review Date: 2009-11-23 |
Journal Detail:
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Title: Clinical and experimental pharmacology & physiology Volume: 37 ISSN: 1440-1681 ISO Abbreviation: Clin. Exp. Pharmacol. Physiol. Publication Date: 2010 Apr |
Date Detail:
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Created Date: 2010-04-22 Completed Date: 2010-08-06 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0425076 Medline TA: Clin Exp Pharmacol Physiol Country: Australia |
Other Details:
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Languages: eng Pagination: 516-24 Citation Subset: IM |
Affiliation:
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School of Biomedical Sciences, Faculty of Health, University of Newcastle, Callaghan, New South Wales, Australia. dirk.vanhelden@newcastle.edu.au |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Biological Clocks / drug effects, physiology Calcium / metabolism Calcium Signaling / drug effects Humans Interstitial Cells of Cajal / drug effects, physiology Models, Biological Muscle Contraction / drug effects, physiology* Muscle, Smooth / drug effects, innervation Myenteric Plexus / physiology Neural Conduction / drug effects Peristalsis / drug effects, physiology* Stomach / drug effects, innervation*, physiology* |
| Chemical | |
Reg. No./Substance:
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7440-70-2/Calcium |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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