2000
DOI: 10.1016/s1566-0702(00)00206-x
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Constitutive nitric oxide release modulates neurally-evoked chloride secretion in guinea pig colon

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Cited by 8 publications
(7 citation statements)
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“…These data suggest that NO plays a physiological role in modulating nicotinic receptor-mediated cholinergic ion transport in the mouse colon and that this role becomes more prominent during inflammation associated with dysfunctional epithelial muscarinic cholinergic receptors. Such a possibility is supported by evidence showing that NO suppresses electrically evoked ion transport mediated by submucosal neurons in the guinea pig colon (31).…”
Section: Fluorescence Micrographs Of Inos and Glial Fibrillatory Acmentioning
confidence: 87%
“…These data suggest that NO plays a physiological role in modulating nicotinic receptor-mediated cholinergic ion transport in the mouse colon and that this role becomes more prominent during inflammation associated with dysfunctional epithelial muscarinic cholinergic receptors. Such a possibility is supported by evidence showing that NO suppresses electrically evoked ion transport mediated by submucosal neurons in the guinea pig colon (31).…”
Section: Fluorescence Micrographs Of Inos and Glial Fibrillatory Acmentioning
confidence: 87%
“…Nitric oxide (NO) is tonically produced under physiological conditions by the constitutively expressed nitric oxide synthase (NOS) I (neuronal NOS), and in higher amounts during inflammation when inducible NOS II (inducible NOS) is mobilized (Moncada & Bolanos, 2006). Nitric oxide liberated from a variety of cell types including neurons can affect enteric epithelial ion transport by acting directly upon the epithelium and through the submucosal plexus of the ENS (Tamai & Gaginella, 1993; Wilson et al 1993; Rao et al 1994; Stack et al 1996; Mourad et al 1999; Rolfe & Milla, 1999; Reddix et al 2000). NO synthases have been identified within the myenteric plexus, in populations of enteric neurons which express NOS I and in enteric glia which express NOS II under basal conditions (Sang & Young, 1996; Neunlist et al 2001; Green et al 2004; Qu et al 2008).…”
Section: Introductionmentioning
confidence: 99%
“…30). Vice versa, inhibition of NO synthesis by NOS-1 blockade enhanced the effect of electric field stimulation on anion secretion in guinea pig colon (19), and in guinea pig small intestinal myenteric neurons NO inhibited slow excitatory postsynaptic potentials (28). Consequently, NO seems to exert in generally an inhibitory action on enteric neurons, an effect that might be explained by the present observation that the stimulation of Ca 2ϩ influx via voltage-dependent Ca 2ϩ channels causes the opening of Ca 2ϩ -dependent K ϩ channels and thereby hyperpolarizes the membrane (Fig.…”
Section: Discussionmentioning
confidence: 97%
“…In guinea pig small intestine, a NO donor such as sodium nitroprusside (SNP) did not affect basal membrane potential of myenteric neurons but inhibited slow excitatory postsynaptic potentials (28). Furthermore, inhibition of NOS-1 potentiated the effect of electric field stimulation on anion secretion in guinea pig colon, suggesting a basal inhibitory effect of NO on the enteric nervous system (19). In the small intestine of the same species, NO has been reported to act as a retrograde transmitter released from interneurons affecting synaptic transmission between these interneurons and sensory neurons (38).…”
mentioning
confidence: 99%