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. 1999 Feb;44(2):143–147. doi: 10.1136/gut.44.2.143

Role of nitric oxide in intestinal water and electrolyte transport

F MOURAD 1, J TURVILL 1, M FARTHING 1
PMCID: PMC1727394  PMID: 9895365

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Figure 1 .

Figure 1

Putative mechanisms of action of nitric oxide (NO) as a mediator of intestinal water and electrolyte transport under resting conditions. The release of background levels of NO modulates absorption by maintaining microvascular villus perfusion (1); by a direct action on epithelial cell function (2) and tight junction integrity (3); and by the activation of neurotransmission within the enteric nervous system (4). Raised NO concentrations mediate secretion by a direct action on epithelial cell function (or by cyclooygenase- and 5-hydroxytryptamine dependent pathways) (A); and by neurotransmission within the enteric nervous system (B) and the autonomic nervous system (C). 


Figure 2 .

Figure 2

Putative mechanisms of action of nitric oxide (NO) as a mediator of intestinal water and electrolyte transport in hypersecretory states. The inhibition of NO release inhibits secretion by: modulating microvascular villus perfusion (1); a direct action on epithelial cell function (2); the activation of neurotransmission within the enteric nervous system (myenteric plexus) (3) and the autonomic nervous system (4); and by the inhibition of free radical formation (5). Increased levels of NO inhibit secretion by a direct action on epithelial cell function (A) by: the stabilisation of enterochromaffin cells (B) and mast cells (C); inhibiting 5-hydroytryptamine (5-HT) induced secretion (D); and by inhibiting intestinal motility (E). 


Figure 3 .

Figure 3

Putative actions of nitric oxide (NO) on the enterocyte. Actions of NO on the enterocyte include the maintenance of tight junctional integrity (1); the modulation of cell respiration (2); the activation of soluble guanylate cyclase (GC) (3); the opening of apical chloride channels (4); the activation of basolateral potassium channels (5); the stimulation of cyclooxygenase activity to generate prostaglandins (PG) (6); and the modulation of receptor activity (7). 


Selected References

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