Submucosal plexus and electrolyte transport across rat colonic mucosa.

Andres, H.; Rock, R.W.; Bridges, Robert J.; Rummel, W.; Schreiner, Jochen

doi:10.1113/jphysiol.1985.sp015746

Cited by 122 publications

(64 citation statements)

References 24 publications

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“…This suggests that PGE2 may regulate hexose absorption and metabolism by influencing submucosal release of neurotransmitters from the enteric neural network. Spontaneously active neurons from the submucosal plexus are thought to have a direct or indirect inhibitory influence on the mucosa (Andres, Bock, Bridges, Rummel & Schreiner, 1985;Ahsan, Naftalin & Smith, 1988). Certainly, we observed that a-MG uptake by isolated epithelial cells in the present study was enhanced by carbachol and noradrenaline.…”

Section: Resultssupporting

confidence: 63%

A submucosal mechanism of action for prostaglandin E2 on hexose absorption and metabolism in mouse intestine.

Dempster¹,

Kellett²

1992

The Journal of Physiology

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SUMMARY1. The involvement of prostaglandin E2 (PGE2) in hexose absorption and metabolism was studied in mouse small intestinal villus cells.2. Phlorizin-sensitive, Na+-dependent a-methyl-D-glucoside (a-MG) uptake (0-8 mM) during 2 min cell incubations (37 'C) was 74+4 nmol (mg protein)-'. Maximal uptake was 110+8 nmol (mg protein)-', representing an accumulation of 50-fold. Metabolism of D-glucose (5 mM) to L-lactate was 38 nmol min' (mg protein)-'.3. Incubation of isolated cells with indomethacin or PGE2 did not affect a-MG uptake or D-glucose metabolism. By including indomethacin during cell isolation from whole intestine, a-MG uptake was inhibited dose dependently (50-250 /M) by up to 70% (P < 0-001). PGE2 present during both isolation and incubation inhibited by 85 % (P < 0-001 ) at 1 #tM and by 27 % (P < 0 05) at 0-1 M, with no effect at lower concentrations. ac-MG uptake was reduced to 38% (P < 0-01) when 1 /LM-PGE2 and 250 /M-indomethacin were presented in combination. When present during cell isolation and incubation, 1 gzM-PGE2 inhibited lactate production by 24 % (P < 0 05), except when present in combination with 250 ,tm-indomethacin. Indomethacin, itself, had no effect on lactate production. 4. A submucosal mechanism is proposed to account for the observed inhibitory effects of PGE2 on brush-border uptake of x-MG and cellular lactate production. Indomethacin appears to exert not only an effect of its own, possibly via PGindependent actions within the submucosa, but at high concentrations also disrupts the effects of exogenously applied PGE2.

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Section: Resultssupporting

confidence: 63%

A submucosal mechanism of action for prostaglandin E2 on hexose absorption and metabolism in mouse intestine.

Dempster¹,

Kellett²

1992

The Journal of Physiology

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“…Indeed, TTX had no effect on net Na+ or C1-fluxes in distal colonic tissues of 6-to 10-wk-old weaned pigs (18), although the neurotoxin appears to have variable effects on basal Isc (19). In other intestinal tissues in which a significant effect of TTX on basal Isc has been observed, addition of the neurotoxin increases Na+ and Cl-absorption (20)(21)(22)(23). This suggests that in the basal state, ongoing activity of submucosal neurons limits the absorptive capacity of the epithelium for these ions (20,23).…”

Section: Efs Carb Ne 5-htmentioning

confidence: 99%

Developmental Changes in Neurally Mediated Ion Transport in Piglet Distal Colon

Bach

Carey

1994

Pediatr Res

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To better understand the role of cnteric nerves in the regulation of colonic ion transport in neonates, we examined the effects of endogenous and exogenous neurcltransmitters on ion transport across distal colonic tissues of piglets. Tissues were obtained from full-term fetuses; newborns; suckling piglets killed 1 d, 5 d, and 14 d after birth; and 21-d-old piglets that had been weaned for 2 d. Colonic tissues were stripped of external muscle layers and mounted in Ussing flux chambers. Short-circuit current (Isc), a measure of active ion transport, and transmural potential difference were lowest in fetal colons and increased during postnatal development. Tissue conductance remained constant throughout development until d 14 and then rose sharply after weaning. Blockade of enteric neural transmission with tetrodotoxin reduced basal Isc compared with control tissues in fetal, newborn, and 1-d-old piglets but had no effect in older animals. The Na+-channel blocker amiloride had no effect on basal Isc in fetal tissues but significantly reduced Isc in all other groups, with the effect increasing with age. Isc responses to electrical field stimulation of cnteric neurons were similar in fetal throughThe extrinsic and intrinsic nerves that innervate the gastrointestinal tract are important modulators of intestinal ion transport (1, 2). Neuromodulation of intestinal transport is a key w a y in which the gut processes sensory information from luminal and systemic stimuli and initiates appropriate effector mechanisms that maintain the proper consistency and composition of luminal contents (1). Although a number of studies have now identified neural pathways and specific neurotransmitters that regulate transport function, virtually all of these reports have focused o n adult animals o r humans o r at least young animals that have already been weaned. Consequently, apart from the study by Carey and Cooke (3) in 14-d-old piglets and then increased after weaning. Increases in Isc after serosal additions of carbachol (10 KM), serotonin (10 pM), or norepinephrine (10 FM) in fetal and newborn piglets were as great or greater than in the older piglets. For serotonin and norepinephrine, Isc responses rose sharply immediately after weaning. In 1-d-old piglets, Isc responses to all stimuli wcre reduced significantly by removal of C I ions from the bathing solutions. At all ages Isc responses wcre inhibited by bumctanide (10 FM) but were not affected by amiloride. These results demonstrate that colonic CI secretion evoked by endogenous or exogenous addition of neurotransmitters is well developed at an early age in piglets. The aim of the present study w a s t o examine the effects of endogenous and exogenous neurotransmitters o n colonic ion transport during postnatal development in piglets. Although the role of hormonal signals, particularly aldosterone, in mediating developmental changes in colonic ion transport has been studied in several species (4-lo), the effect of enteric neurotransmitters o n colonic

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“…Recent studies indicate that enteric nerves, especially submucosal nerves, influence electrolyte transport in the colon (Ander, Bock, Bridges, Rummel & Schreiner, 1985;Rangachari & McWade, 1986;Kuwahara, Bowen, Wang, Condon & Cooke, 1987).…”

Section: Introductionmentioning

confidence: 99%

Luminal propionate‐induced secretory response in the rat distal colon in vitro.

Yajima

1988

The Journal of Physiology

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SUMMARY1. The stimulatory action of propionate on colonic electrolyte transport and involvement of the enteric reflex in this was studied in vitro using an Ussing chamber in the rat. The short-circuit current (I.,) and bidirectional fluxes of Na+ and Cl-were measured. Mucosa-submucosa preparations, containing the submucosal nerve, from the distal colon were used in most cases.2. Mucosal application of propionate caused transient increases in the transmural potential difference, with the mucosal side negative, ISc and conductance. Serosal application of the acid had no effect.3. Adaptation of the ISC response occurred when the acid was applied to the bathing solution cumulatively without washing out the first dose. If tissues were washed and held more than 20 min before the next application, the response was almost completely restored.4. The increase in IS. in response to propionate was concentration dependent, with a 50% effective concentration of approximately 7 x 10-5 M.5. Two other short-chain fatty acids (SCFAs), n-butyrate and n-valerate, but not acetate, increased ISC when added to the mucosal bathing solution.6. Bumetanide (3 x 10-5 M) and the serosal chloride-free condition, but not amiloride (10-M), inhibited the responses of ISC to propionate. Propionatestimulated Cl-secretion resulted mainly from an increase in unidirectional serosalto-mucosal C1-movement. Propionate did not affect the Na+ flux.7. Tetrodotoxin (10-7 M), somatostatin (10-7 M) and hexamethonium (10-4 M) inhibited the propionate-evoked increase in ISC by 40, 70 and 30°%, respectively.8. Atropine (10-5 M) also inhibited the I,,-increase response to propionate more than 90 %.9. Pre-treatment (2 min) of the mucosal surface with procaine (5 x 10-M)inhibited the propionate-evoked increase in IS. by 90°%.10. The results suggest that luminal propionate transiently stimulated the colonic chloride secretory response that is not due to direct action on colonocytes, but due in large part to release of acetylcholine at neuro-colonocyte junctions, probably via an enteric reflex involving a mucosal sensory mechanism, cholinergic motor nerves and submucosal ganglia.

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Submucosal plexus and electrolyte transport across rat colonic mucosa.

Cited by 122 publications

References 24 publications

A submucosal mechanism of action for prostaglandin E2 on hexose absorption and metabolism in mouse intestine.

A submucosal mechanism of action for prostaglandin E2 on hexose absorption and metabolism in mouse intestine.

Developmental Changes in Neurally Mediated Ion Transport in Piglet Distal Colon

Luminal propionate‐induced secretory response in the rat distal colon in vitro.

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