Textbook of Gastroenterology 2008
DOI: 10.1002/9781444303254.ch47
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Dysmotility of the Small Intestine and Colon

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Cited by 6 publications
(5 citation statements)
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“…Double-knockout mice for CFTR and CLC-2 produce a lower apparent rate of K + secretion compared with CFTR knockout mice, suggesting that CLC-2 contributes to basolateral Cl − conductance involved in K + secretion (Zdebik et al 2004). Another manifestation of K + secretion appears in patients with acute colonic pseudo-obstruction (Jetmore et al 1992;Camilleri & Szarka, 2009). The K + wasting observed (van Dinter et al 2005;Blondon et al 2008) probably results from prolonged sympathetic activation of K + secretion.…”
Section: Discussionmentioning
confidence: 99%
“…Double-knockout mice for CFTR and CLC-2 produce a lower apparent rate of K + secretion compared with CFTR knockout mice, suggesting that CLC-2 contributes to basolateral Cl − conductance involved in K + secretion (Zdebik et al 2004). Another manifestation of K + secretion appears in patients with acute colonic pseudo-obstruction (Jetmore et al 1992;Camilleri & Szarka, 2009). The K + wasting observed (van Dinter et al 2005;Blondon et al 2008) probably results from prolonged sympathetic activation of K + secretion.…”
Section: Discussionmentioning
confidence: 99%
“…Partial degeneration of the enteric nervous system during life leads to severe dysmotility. Such degeneration occurs, for example, when the enteric nervous system is targeted by the infective organism of Chagas disease, Trypanosoma cruzi [2]. The enteric nervous system circuits have essential roles in the control of motility, blood flow, water and electrolyte transport, and acid secretion in the digestive tract, and the enteric nervous system is most commonly the medium through which extrinsic neurons control gastrointestinal function [3].…”
Section: Locations Of the Enteric Gangliamentioning
confidence: 99%
“…Excitatory circular muscle motor neurons (6) Inhibitory circular muscle motor neurons (7) Excitatory longitudinal muscle motor neurons (4) Inhibitory longitudinal muscle motor neurons (5) Excitatory neurons to the muscularis mucosae Inhibitory neurons to the muscularis mucosae Myenteric ascending interneurons (1) Myenteric descending interneurons (local reflex) (8) Myenteric descending interneurons (secretomotor and motility reflexes) (9) Myenteric descending interneurons (MMC) (10) Myenteric intrinsic primary afferent neurons (IPANs) (2) Submucosal IPANs (11) Intestinofugal neurons (3) Motor neurons to gut endocrine cells Noncholinergic secretomotor/ vasodilator neurons (12) Cholinergic secretomotor/vasodilator neurons (13) Cholinergic secretomotor (nonvasodilator) neurons (14) Submucosal uniaxonal neurons projecting to the myenteric plexus (15) ACh, acetylcholine; ATP, adenosine triphosphate; CGRP, calcitonin gene-related peptide; GRP, gastrin-releasing peptide; 5-HT, 5-hydroxytryptamine; MMC, migrating myoelectric complex; NK, neurokinin (receptor); NO, nitric oxide; NOS, nitric oxide synthase; PACAP, pituitary adenylyl cyclase-activating peptide; TK, tachykinin; VIP, vasoactive intestinal peptide.…”
Section: Functional Definitionmentioning
confidence: 99%
“…The absence of Cl Ϫ secretion from these responses illustrates the underlying capacity to produce modulatory secretion. In those aCPO patients having high fecal K ϩ concentrations (9,13,41,67), hypokalemia likely results from inappropriately prolonged modulatory secretion. The accompanying colonic distension caused by the dominance of sympathetic over parasympathetic influences on gut motility provides a large reservoir for K ϩ accumulation from the continual K ϩ secretion, likely activated via a ␤ 1 -AdrR/␤ 2 -AdrR complex (74).…”
mentioning
confidence: 99%