Indirect effects of bradykinin on ion transport in rat colon descendens: mediated by prostaglandins and enteric neurons

1988 ◽  
Vol 337 (1) ◽  
Author(s):  
M. Diener ◽  
R.J. Bridges ◽  
S.F. Knobloch ◽  
W. Rummel
Keyword(s):  
Ion Transport ◽  
Indirect Effects ◽  
Enteric Neurons ◽  
Rat Colon

Neural regulation of in vitro giant contractions in the rat colon

2001 ◽  
Vol 281 (1) ◽  
pp. G275-G282 ◽  
Author(s):  
Asensio Gonzalez ◽  
Sushil K. Sarna
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Sch 23390 ◽  
Circular Muscle ◽  
Electrical Field Stimulation ◽  
Muscle Cells ◽  
Enteric Neurons ◽  
Rat Colon ◽  
Spontaneous Contractions

The rat middle colon spontaneously generates regularly occurring giant contractions (GCs) in vitro. We investigated the neurohumoral and intracellular regulation of these contractions in a standard muscle bath. cGMP content was measured in strips and single smooth muscle cells. The circular muscle strips generated spontaneous GCs. Their amplitude and frequency were significantly increased by tetrodotoxin (TTX), ω-conotoxin, N ω-nitro-l-arginine (l-NNA), and the dopamine D1 receptor antagonist Sch-23390. The GCs were unaffected by hexamethonium, atropine, and antagonists of serotonergic (5-HT1–4), histaminergic (H1–2), and tachykininergic (NK1–2) receptors but enhanced by NK3receptor antagonism. The guanylate cyclase inhibitor 1H-[1,2,4]oxidiazolo[4,3-a]quinoxalin-1-one (ODQ) also enhanced GCs to the same extent as TTX and l-NNA, and each of the three agents prevented the effects of the others. GCs were abolished by electrical field stimulation, S-nitroso- N-acetyl-penicillamine, and 8-bromo-cGMP. BAY-K-8644 and apamin enhanced the GCs, but they were abolished by D-600. Basal cGMP content in strips was decreased by TTX,l-NNA, or ODQ, but these treatments had no effect on cGMP content of enzymatically dissociated single smooth muscle cells. We conclude that spontaneous contractions in the rat colonic muscle strips are not generated by cholinergic, serotonergic, or histaminergic input. Constitutive release of nitric oxide from enteric neurons sustains cGMP synthesis in the colonic smooth muscle to suppress spontaneous in vitro GCs.

Complement Activation of Electrogenic Ion Transport in Isolated Rat Colon

1997 ◽  
Vol 54 (10) ◽  
pp. 1133-1137 ◽  
Author(s):  
Declan F McCole ◽  
Barbara Otti ◽  
Philip Newsholme ◽  
Alan W Baird
Keyword(s):  
Ion Transport ◽  
Complement Activation ◽  
Rat Colon ◽  
Electrogenic Ion Transport ◽  
Isolated Rat ◽  
Isolated Rat Colon

Oxygen Metabolites in Immune- Stimulated Ion Transport in Rat Colon: Modulation by Taurine

Digestion ◽  
2001 ◽  
Vol 63 (2) ◽  
pp. 124-129 ◽  
Author(s):  
Maeve M. Skelly ◽  
Diarmuid P. O’Donoghue ◽  
Alan W. Baird
Keyword(s):  
Ion Transport ◽  
Rat Colon ◽  
Oxygen Metabolites

scholarly journals Rhubarb-Evoke Mucus Secretion through Aggregation and Degranulation of Mast Cell in the Colon of Rat: In vivo and ex vivo studies

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Di Wu ◽  
Xiaowei Xue ◽  
Chenchen Gao ◽  
Yuehong Liu ◽  
Tiantian Wang ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Water Content ◽  
Cell Activation ◽  
Ex Vivo ◽  
Mucus Secretion ◽  
Enteric Neurons ◽  
Mast Cell Activation ◽  
Rat Colon

AbstractRhubarb is commonly used to treat constipation in China for its function of promoting intestinal movement and optimum water content in feces. However, its mechanism of mucus secretion is vague. The aim of the study is to investigate the role of mast cells and enteric neurons in rhubarb extract (RE)-induced mucus secretion in the rat colon. Immunofluorescence was used to detect histamine receptors. Western blotting and 3,3′-diaminobenzidine (DAB) were applied to explore the content changes of mast cells activation. The changes in colonic goblet cells (GCs) were determined by means of PAS/AB staining. An intestinal perfusion system with a Bradford protein assay kit was directly to estimate in vitro secretion. And the cytokines were investigated with ELISA. The longitudinal aspect of this study indicate that the number and water content of faecal pellets were enhanced after the administration of different doses of RE accompanied by mast cells accumulated and increased the content of interferon (IFN) -γ or decreased the levels of interleukin (IL) −10 at doses of 3 and 6 g/kg. Pretreatment with ketotifen, mast cell stabilizer, had partially inhibited on RE-induced mucus secretion. Furthermore, RE induced the release of acetylcholine and mucin-2 in the colonic tissue and the histamine levels from the faeces. The results suggest that RE induced colonic mucus secretion involves mast cell activation and some cytokine.

Tachykinin NK2 receptor mediates contraction and ion transport in rat colon by different mechanisms

2001 ◽  
Vol 415 (2-3) ◽  
pp. 277-283 ◽  
Author(s):  
Riccardo Patacchini ◽  
Helen M Cox ◽  
Sandra Ståhl ◽  
Iain R Tough ◽  
Carlo Alberto Maggi
Keyword(s):  
Ion Transport ◽  
Rat Colon ◽  
Nk2 Receptor ◽  
Tachykinin Nk2 Receptor

scholarly journals Acute regulation of intestinal ion transport and permeability in response to luminal nutrients: the role of the enteric nervous system

2020 ◽  
Vol 318 (2) ◽  
pp. G254-G264
Author(s):  
Jean-Baptiste Cavin ◽  
Hailey Cuddihey ◽  
Wallace K. MacNaughton ◽  
Keith A. Sharkey
Keyword(s):  
Nervous System ◽  
Small Intestine ◽  
Ion Transport ◽  
Enteric Nervous System ◽  
Intestinal Permeability ◽  
Barrier Function ◽  
Enteric Neurons ◽  
Nerve Activity ◽  
Mouse Small Intestine

The small intestine regulates barrier function to absorb nutrients while avoiding the entry of potentially harmful substances or bacteria. Barrier function is dynamically regulated in part by the enteric nervous system (ENS). The role of the ENS in regulating barrier function in response to luminal nutrients is not well understood. We hypothesize that the ENS regulates intestinal permeability and ion flux in the small intestine in response to luminal nutrients. Segments of jejunum and ileum from mice were mounted in Ussing chambers. Transepithelial electrical resistance (TER), short-circuit current ( Isc), and permeability to 4-kDa FITC-dextran (FD4) were recorded after mucosal stimulation with either glucose, fructose, glutamine (10 mM), or 5% Intralipid. Mucosal lipopolysaccharide (1 mg/mL) was also studied. Enteric neurons were inhibited with tetrodotoxin (TTX; 0.5 μM) or activated with veratridine (10 μM). Enteric glia were inhibited with the connexin‐43 blocker Gap26 (20 μM). Glucose, glutamine, Intralipid, and veratridine acutely modified Isc in the jejunum and ileum, but the effect of nutrients on Isc was insensitive to TTX. TTX, Gap26, and veratridine treatment did not affect baseline TER or permeability. Intralipid acutely decreased permeability to FD4, while LPS increased it. TTX pretreatment abolished the effect of Intralipid and exacerbated the LPS‐induced increase in permeability. Luminal nutrients and enteric nerve activity both affect ion flux in the mouse small intestine acutely but independently of each other. Neither neuronal nor glial activity is required for the maintenance of baseline intestinal permeability; however, neuronal activity is essential for the acute regulation of intestinal permeability in response to luminal lipids and lipopolysaccharide. NEW & NOTEWORTHY Luminal nutrients and enteric nerve activity both affect ion transport in the mouse small intestine acutely, but independently of each other. Activation or inhibition of the enteric neurons does not affect intestinal permeability, but enteric neural activity is essential for the acute regulation of intestinal permeability in response to luminal lipids and lipopolysaccharide. The enteric nervous system regulates epithelial homeostasis in the small intestine in a time-dependent, region- and stimulus-specific manner.

scholarly journals Effects of acid-base variables on ion transport in rat colon.

1988 ◽  
Vol 81 (6) ◽  
pp. 1903-1910 ◽  
Author(s):  
D S Goldfarb ◽  
R W Egnor ◽  
A N Charney
Keyword(s):  
Ion Transport ◽  
Rat Colon ◽  
Acid Base

Mechanism of cholinergic regulation of electrolyte transport in rat colon in vitro

1982 ◽  
Vol 242 (2) ◽  
pp. G116-G123 ◽  
Author(s):  
T. W. Zimmerman ◽  
J. W. Dobbins ◽  
H. J. Binder
Keyword(s):  
Ion Transport ◽  
Chloride Transport ◽  
Short Circuit ◽  
Electrolyte Transport ◽  
Rat Colon ◽  
Bathing Solution ◽  
Camp Content ◽  
Cholinergic Regulation ◽  
Chloride Absorption

Cholinergic agonists inhibit sodium and chloride absorption in the intestine and often produce secretion. To determine the mechanism of cholinergic regulation of intestinal electrolyte transport, the effects of bethanechol on ion transport were studied in the rat colon in vitro. The addition of 1 mM bethanechol produced an initially large but short-lived increase in short-circuit current (Isc) (171 +/- 19 microA/cm2). Bethanechol decreased net sodium and net chloride absorption (2.5 +/- 0.5 and 2.9 +/- 0.9 mueq . h-1 . cm-2, respectively) and increased Isc (0.8 +/- 0.3 mueq . h-1 . cm-2) during the steady-state period. All these effects were inhibited by 1 microM atropine, which alone had no effect on ion transport. The removal of either sodium or chloride also inhibited the effect of bethanechol. cAMP content did not increase in isolated enterocytes incubated with bethanechol; however, calcium removal from the serosal bathing solution inhibited the bethanechol-induced changes in ion transport. These results indicate that cholinergic muscarinic agonists alter sodium and chloride transport in the colon by inhibiting coupled NaCl absorption by a calcium-dependent, non-cAMP-mediated process.

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