The enteric nervous system participates in the secretory response to the heat stable enterotoxins of Escherichia coli in rats and cats

Eklund, Stefan; Jodal, Mats; Lundgren, Ove

doi:10.1016/0306-4522(85)90318-5

Cited by 92 publications

(65 citation statements)

References 19 publications

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“…The results confirm that carbachol and STa, when added simultaneously, induce a supra-additive or synergistic increase in Isc compared to each agonist added alone***. These results may also provide an explanation for previous, poorly understood in vivo observations showing inhibition of STa-induced secretion in intestinal segments by cholinergic blockers in rats and cats [27]. Thus the interaction of carbachol and STa may have important physiologic implications, since the enteric nervous system and gastrointestinal hormones which raise intracellular calcium could affect one's susceptibility to diarrhea due to toxigenic Escherichia coli.…”

Section: Discussionsupporting

confidence: 82%

Carbachol mimics phorbol esters in its ability to enhance cyclic GMP production by STa, the heat‐stable toxin of Escherichia coli

et al. 1990

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STa, the heat-stable enterotoxin of Escherichia coli, stimulates membrane-bound guanylate cyclase in enterocytes, elevates cyclic GMP, and results in intestinal secretion of ions and fluid. Using the T84 colon carcinoma cell line as a model, Weikel et al. reported that phorbol esters enhance STa-stimulated cyclic GMP production by 61%140% ) Infect. Immun. 58, 1402 1407. In the present report we demonstrate that the acetylcholine analog carbachol enhanced toxin-stimulated cyclic GMP accumulation in intact T84 cells by 50-100% and that this effect was blocked by 10 /~M atropine and 10/IM sphingosine. Pertussis toxin treatment of the T84 cells did not affect the subsequent response to carbachol. Carbachol, which elevates intracellular calcium in these cells, may act through protein kinase C to enhance cyclic GMP production.

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Section: Discussionsupporting

confidence: 82%

Carbachol mimics phorbol esters in its ability to enhance cyclic GMP production by STa, the heat‐stable toxin of Escherichia coli

et al. 1990

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“…As a result of the observed inhibition of basal fluid absorption (in the cat) from luminally instilled lidocaine, in further studies Cassuto and co-workers applied the anaesthetic on to the serosal surface of the jejunum, where it was found to inhibit CTinduced secretion in the cat and rat, as it did on the mucosal side, but was claimed not to interfere with basal fluid absorption in either animal (Cassuto, Siewert, Jodal & Lundgren, 1983). The serosal application of lidocaine was found also to inhibit the jejunal fluid secretion induced by luminal STa in fed rats (Eklund et al 1985). On the basis of this and the inhibition by other neuroantagonists, Eklund et al (1985) proposed that luminal STa, like CT-induced secretion, activated secretion not only by a direct action on the enterocytes but also by an indirect neural reflex.…”

Section: Chemicalsmentioning

confidence: 91%

Fluid hypersecretion induced by enterotoxin STa in nutritionally deprived rats: jejunal and ileal dynamics in vivo

Nzegwu¹,

Levin²

1994

Experimental Physiology

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SUMMARYThe effect of luminal enterotoxin Escherichia coli STa on fluid transport across the jejunum and ileum of fed, starved (72 h) and chronically undernourished (50 % control food intake for 21 days) rats was assessed in vivo using a gravimetric technique. Dose-response curves for net fluid secretion (stimulated -basal (30 min)-') activated by 5, 50 and 500 ng ml-' STa were obtained for jejuna and ilea from fed, starved and chronically undernourished rats. Compared to the fed rats, both dietary deprivations showed enhanced net fluid secretion at 500 ng ml-1, but only the jejunum from chronically undernourished rats showed significantly enhanced secretion at 5 and 50 ng ml-1. Net fluid secretory responses to a standard dose of STa (500 ng ml-1) were monitored in the jejuna and ilea of fed, starved and chronically undernourished rats at 30, 60, 90 and 120 min. The pattern in jejuna and ilea from fed rats was very different; the jejunal secretion over 30 min was transient, but ileal secretion increased continuously to a maximum at 120 min. In both jejunum and ileum from starved rats, the secretory response to STa at 30 min was significantly greater than that in fed rats and subsequently remained near this level. In the jejunum from chronically undernourished rats, the net fluid secreted in response to STa was greatly enhanced at 30 and 60 min, but not at 90 min. The ileal response was significantly greater than that in the fed rats at 30 and 120 min. Luminal procaine (10 mM) selectively increased fluid absorptive tone in the jejunum from fed rats, reduced STa-induced fluid secretion in the ileum from undernourished rats, but had no effect on STa in the jejunum from undernourished rats or in the jejunum or ileum from starved rats. Luminal 8-bromo-cyclic GMP (1 mM) had no effect on basal absorptive tone in the jejunum of fed or chronically undernourished rats, but enhanced the secretory tone of jejunum from starved rats. In the ileum, however, while 8-bromo-cyclic GMP enhanced secretory tone in the fed and starved conditions, it still had no action in the chronically undernourished state. The enhanced fluid secretion observed in the jejunum and ileum of the starved and undernourished rats compared to the fed rats supports previous in vitro findings of an increased electrogenic secretion induced by STa in these dietary deprivations. The fluid hypersecretion could be a cause of the increased severity of diarrhoea often observed in undernourished and starved humans.

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“…Moreover, the participation of enteric nerves and arachidonic acid metabolites in the mediation of NO effects is proposed (Wilson et al, 1993;Tamai & Gaginella, 1993;Takeuchi et al, 1993). Similar mechanisms of signal transduction have been shown to be involved in the mediation of fluid secretion induced by Escherichia coli heat stable enterotoxin a (E. coli STa): the enterotoxin elevates intestinal cyclic GMP levels (Hughes et al, 1978) and involves prostaglandins (Thomas & Knoop, 1982) and the enteric nervous system (Eklund et al, 1985) in its mechanism of action. In addition, 5-hydroxytryptamine (5-HT) has also been demonstrated to participate in the mediation of E. coli STa-induced fluid secretion (Beubler et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

Significance of nitric oxide in the stimulation of intestinal fluid absorption in the rat jejunum in vivo

Schirgi‐Degen

Beubler

1995

British J Pharmacology

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1 The effects of inhibiting nitric oxide (NO)-synthase on fluid transport, mucosal cyclic GMP and cyclic AMP levels and intraluminal prostaglandin E2 (PGE2)-release were studied in a model of ligated jejunal loops of anaesthetized rats in vivo. Experiments were performed under basal conditions as well as under conditions, when net fluid secretion was induced by Escherichia coli heat stable enterotoxin a (E. coli STa) or PGE2. 2 Intravenous infusion of the NO-synthase inhibitor N0-nitro-L-arginine methyl ester (L-NAME, 0.25-50mgrkg-', 45min) dose-dependently reversed net fluid absorption to net secretion, whereas infusion of D-NAME, the inactive enantiomer of L-NAME, in corresponding doses did not influence net fluid transport. Nw-nitro-L-arginine (L-NOARG, 25 mg kg-'), another NO-synthase inhibitor, also elicited net secretion of fluid. -3 L-NAME (25 mg kg ')-induced net fluid secretion was reversed to net absorption by infusion of L-arginine (400 mg kg') or sodium nitroprusside (1 mg kg-') and s.c. administration of indomethacin (10 mg kg-'). Hexamethonium (1 mg kg-', s.c.), a ganglionic blocker and granisetron (100 gsg kg-', s.c.), a 5-HT3-receptor antagonist, did not influence L-NAME-induced net secretion. 4 Net fluid secretion induced by intraluminal instillation of E. coli STa (10 units ml-') was enhanced by infusion of L-NAME (25mgkg-') and was inhibited by infusion of L-arginine (400mgkg-') and sodium nitroprusside (1 mg kg-'). D-Arginine (400 mg kg-') did not influence E. coli STa-induced fluid secretion. Likewise, net fluid secretion induced by i.a. infusion of PGE2 (79 ng ml-, 30 min) was enhanced by infusion of L-NAME and was inhibited by L-arginine and sodium nitroprusside. D-Arginine (400 mg kg-') did not influence PGE2-induced fluid secretion. 5 PGE2 levels in intraluminal fluid were not elevated after infusion of L-NAME (25mgkg-') compared to controls. 6 Mucosal cyclic GMP and cyclic AMP levels after L-NAME-treatment were not different from control values. 7 These results indicate that nitric oxide plays an important role in the regulation of intestinal fluid transport. The data suggest a nitric oxide-dependent proabsorptive tone in the intestine, which possibly involves the enteric nervous system and suppression of prostaglandin formation. This proabsorptive tone also may downregulate fluid secretion induced by E. coli STa or PGE2.

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The enteric nervous system participates in the secretory response to the heat stable enterotoxins of Escherichia coli in rats and cats

Cited by 92 publications

References 19 publications

Carbachol mimics phorbol esters in its ability to enhance cyclic GMP production by STa, the heat‐stable toxin of Escherichia coli

Carbachol mimics phorbol esters in its ability to enhance cyclic GMP production by STa, the heat‐stable toxin of Escherichia coli

Fluid hypersecretion induced by enterotoxin STa in nutritionally deprived rats: jejunal and ileal dynamics in vivo

Significance of nitric oxide in the stimulation of intestinal fluid absorption in the rat jejunum in vivo

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