The role of nitric oxide in the regulation of colonic water and electrolyte transport in normal colon and during acetic acid experimental colitis in rats

Impairment of small intestinal absorption has been described in patients with ulcerative colitis and in animal models of experimental colitis. The pathophysiology of this dysfunction has not been elucidated. The aim of this study was to investigate the effect of chemical colitis on jejunal fluid absorption and determine the role of the enteric nervous system and some putative neurotransmitters. In a rat model of iodoacetamide-induced colitis, jejunal net fluid absorption was evaluated by the in vivo single-pass perfusion technique. The effects of 1) tetrodotoxin (TTX), 2) benzylalkonium chloride (BAC), 3) capsaicin, 4) vasoactive intestinal polypeptide (VIP) antagonism, 5) nitric oxide (NO) synthase (NOS) inhibition, and 6) 5-hydroxytryptamine type 3 and 4 (5-HT3 and 5-HT4) receptor antagonism on the changes in fluid movement were investigated. A significant decrease in jejunal net fluid absorption was found 2 and 4 days after colitis induction: 26 (SD 14) and 28 (SD 19) μl·min−1·g dry intestinal wt−1, respectively [ P < 0.0002 compared with sham rats at 61 (SD 6.5) μl·min−1·g dry intestinal wt−1]. No histological changes were evident in jejunal sections. TTX and BAC reversed this decrease in fluid absorption: 54 (SD 13) and 44 (SD 14) μl·min−1·g dry intestinal wt−1 ( P = 0.0005 and P = 0.019, respectively, compared with colitis). Ablation of capsaicin-sensitive primary afferent fibers had a partial effect: 45 (SD 5) μl·min−1·g dry intestinal wt−1 ( P = 0.001 and P = 0.003 compared with colitis and sham, respectively). Constitutive and neuronal NOS inhibition and VIP antagonism returned jejunal net fluid absorption to normal values: 66 (SD 19), 61 (SD 5), and 56 (SD 14) μl·min−1·g dry intestinal wt−1, respectively. 5-HT3 and 5-HT4 receptor antagonism had no effect. Chemical colitis is associated with a significant decrease in jejunal net fluid absorption. This decrease is neurally mediated and involves VIP- and NO-related mechanisms.

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Protective vascular effects of quercitrin in acute TNBS-colitis in rats: the role of nitric oxide

Food & Function ◽

10.1039/c7fo00755h ◽

2017 ◽

Vol 8 (8) ◽

pp. 2702-2711 ◽

Cited By ~ 7

Author(s):

Miguel Romero ◽

Beatriz Vera ◽

Milagros Galisteo ◽

Marta Toral ◽

Julio Gálvez ◽

...

Keyword(s):

Nitric Oxide ◽

Experimental Colitis ◽

Inflammatory Activity ◽

Vascular Effects ◽

Tnbs Colitis ◽

Anti Inflammatory

Quercitrin (quercetin 3-rhamnoside) is a bioflavonoid with anti-inflammatory activity in experimental colitis.

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Role of nitric oxide in inflammation-induced suppression of secretion in a mouse model of acute colitis

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1998.275.6.g1353 ◽

1998 ◽

Vol 275 (6) ◽

pp. G1353-G1360 ◽

Cited By ~ 15

Author(s):

Wallace K. MacNaughton ◽

Sonya S. Lowe ◽

Kelly Cushing

Keyword(s):

Nitric Oxide ◽

Short Circuit ◽

Electrolyte Transport ◽

Inos Mrna ◽

Myeloperoxidase Activity ◽

Current Response ◽

Muscarinic Agonist ◽

Trinitrobenzenesulfonic Acid ◽

Ussing Chambers

The role of nitric oxide (NO) derived from the inducible isoform of NO synthase (iNOS) in epithelial transport dysfunction was studied in a model of colitis induced in mice by intrarectal 2,4,6-trinitrobenzenesulfonic acid in 30% ethanol. Expression of iNOS mRNA was determined by RT-PCR. Electrolyte transport studies were conducted in Ussing chambers in which segments of inflamed colon were incubated with or without the selective iNOS inhibitorl- N 6-(1-iminoethyl)lysine (l-NIL). Seven days after the induction of colitis, colonic tissue exhibited increased myeloperoxidase activity compared with saline controls. There was a detectable basal expression of iNOS mRNA, but expression was increased 3.7-fold in inflamed colons. Inflammation also caused an increase in iNOS activity and a concomitant decrease in constitutive NOS activity. In Ussing chamber experiments, there was a decreased response to electrical field stimulation in inflamed tissue, which was partially reversed by pretreatment of the tissue withl-NIL. The short-circuit current response to the muscarinic agonist carbachol was also reduced in inflammation, but this was not reversed byl-NIL. In summary, NO derived from iNOS mediates, in part, inflammation-induced suppression of neurally evoked electrolyte transport.

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Role of nitric oxide in radiation-induced alterations in electrolyte transport in the rat colon in vitro

Gastroenterology ◽

10.1016/0016-5085(95)23743-7 ◽

1995 ◽

Vol 108 (4) ◽

pp. A271

Keyword(s):

Nitric Oxide ◽

Electrolyte Transport ◽

Rat Colon ◽

Radiation Induced

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Role of nitric oxide in the convulsive seizures induced by fluoroquinolones coadministered with 4-biphenyl acetic acid

General Pharmacology The Vascular System ◽

10.1016/s0306-3623(97)00023-2 ◽

1997 ◽

Vol 29 (5) ◽

pp. 767-770 ◽

Cited By ~ 6

Author(s):

Ken-ichi Kohno ◽

Masayuki Niwa ◽

Masakatsu Nozaki ◽

Toshihiko Uematsu ◽

Hajime Fujimura

Keyword(s):

Nitric Oxide ◽

Acetic Acid ◽

Convulsive Seizures

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Effects of N-acetylcysteine Treatment on Oxidative Stress in Acetic Acid-induced Experimental Colitis in Rats

Journal of International Medical Research ◽

10.1177/147323000503300207 ◽

2005 ◽

Vol 33 (2) ◽

pp. 196-206 ◽

Cited By ~ 35

Author(s):

E Akgun ◽

C Çaliskan ◽

HA Celik ◽

AO Ozutemiz ◽

M Tuncyurek ◽

...

Keyword(s):

Nitric Oxide ◽

Acetic Acid ◽

Experimental Colitis ◽

Rat Colon ◽

Protective Effects ◽

Colonic Injury ◽

Toxic Damage ◽

Standard Assay ◽

Inflammatory Bowel ◽

Acid Administration

We assessed the possible protective effects of N-acetylcysteine (NAC) against toxic damage in the rat colon. Two doses of NAC (20 mg/kg and 100 mg/kg) given for 2 days and 7 days after acetic acid administration (to induce colitis) were tested. NAC was dissolved in saline and administered locally (intracolonic), systemically (intraperitoneal) or in a combination (intracolonic and intraperitoneal). Several parameters, including macroscopic and histopathological scores and myeloperoxidase, glutathione and nitric oxide concentrations were measured using standard assay procedures. Treatment with 100 mg/kg NAC for 7 days significantly decreased tissue myeloperoxidase, glutathione and nitric oxide concentrations. The 20 mg/kg dose had no protective effects. The data indicate that NAC substantially reduced the degree of colonic injury, probably by regulating free radical production and inhibiting inflammation. It may, therefore, have a role in the treatment of inflammatory bowel disease.

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