Wyniki wyszukiwania

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Neurally-mediated and neurally-independent beneficial actions of melatonin in the gastrointestinal tract

100%

Reiter R. J., Tan D-X., Mayo J. C., Sainz R. M., Leon J., Bandyopadhyay D.

Journal of Physiology and Pharmacology. Supplement

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2003

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tom 54

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nr 4

113-125

Melatonin (N-acetyl-5-methoxytryptamine), originally discovered in the pineal gland, is now known also to be present in the gastrointestinal tract from the stomach to the colon. It is localized and likely synthesized in the enterochromaffin cells of the mucosal lining. Its functions in the gut generally seem to be protective of the mucosa from erosion and ulcer formation and to possibly influence movement of the gastrointestinal contents through the digestive system. In this brief review, we summarize the work documenting the function of melatonin in influencing bicarbonate secretion in the stomach and its role in preventing and repairing ulcers in the stomach and duodenum. Melatonin’s actions in the control of bicarbonate secretion involve the central and peripheral sympathetic nervous systems and the actions are receptor mediated. Conversely, melatonin’s actions in reducing ulcer formation also seemingly involve the ability of the indole to directly scavenge toxic oxygen-based reactants, e.g., the hydroxyl radical, and possibly to promote antioxidative enzyme activities. These same processes may be involved in the mechanisms by which melatonin promotes ulcer healing. Additionally, however, melatonin’s effects on the healing of ulcers includes actions of blood flow in the margins of the ulcer and also on the sensory nerves. All indications are that melatonin has a variety of beneficial effects in the gastrointestinal tract. It is likely, however, that additional actions of melatonin on the digestive system will be uncovered.

2

Central nervous stimuli increase duodenal bicarbonate secretion by release of mucosal melatonin

100%

Sjoblom M., Flemstrom G.

Journal of Physiology and Pharmacology

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2001

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tom 52

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nr 4,1

A number of common diseases in humans, including gastroduodenal ulcer and irritable bowel syndrome, show circadian rhythms in pain and discomfort. The neurohormone melatonin is released from enterochromaffin cells in the intestinal mucosa and from the pineal gland but its role in gastrointestinal function is largely unknown. We have studied the involvement of melatonin in stimulation of the mucosa-protective alkaline secretion by the duodenal mucosa. A 12-mm segment of proximal duodenum with an intact blood supply was cannulated in situ in anesthetized rats and duodenal HCO3– secretion titrated by pH-stat. Duodenal close intra-arterial infusion of melatonin or the full agonist 2-iodo-N-butanoyl- 5-methoxytryptamine significantly increased the secretion and pretreatment with the melatonin (predominantly MT2-receptor specific) antagonist luzindole almost abolished the response. Intracerebroventricular (i.c.v.) infusion of the alpha1-adrenoceptor agonist phenylephrine (12.2 µmol kg-1·h-1 ) caused an up to fivefold increased in the alkaline secretion and the melatonin antagonist luzindole or cutting all peri-carotid nerves abolished the duodenal secretory response to i.c.v. phenylephrine. Peripheral melatonin thus stimulates duodenal mucosal HCO3 – secretion and endogenous melatonin, very likely released from mucosal enterochromaffin cells, is involved in mediating neural stimulation of the secretion.

3

Vectorial bicarbonate transport by Par-C10 salivary cells

80%

Demeter I., Szucs A., Hegyesi O., Foldes A., Racz G. Z., Burghardt B., Steward M. C., Varga G.

Journal of Physiology and Pharmacology. Supplement

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2009

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tom 60

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nr 7

4

Acid-sensing protective mechanisms of duodenum

80%

Kaunitz J. D., Akiba Y.

Journal of Physiology and Pharmacology. Supplement

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2003

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tom 54

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nr 4

19-26

The proximal duodenal mucosa, exposed to frequent pulses of gastric acid, is functionally "leaky", increasing the importance of defense mechanisms such as the mucus gel layer, cellular acid/base transporters, bicarbonate secretion, and mucosal blood flow. Our laboratory has used a unique in vitro perfused microscopic system to measure thickness of the adherent mucus gel (MGT), intracellular pH (pHi), bicarbonate secretion, and mucosal blood flow in anesthetized rats. Exposure to pulses of luminal acid, mimicking the rapid physiologic shifts of luminal pH, increases MGT and blood flow, and induces cellular bicarbonate loading, the latter followed by augmented bicarbonate secretion. The mechanism by which the epithelium senses luminal acid includes capsazepine-inhibitable vanilloid receptors, presumably similar to the vanilloid receptor TPVR-1. CFTR, the cAMP-regulated anion channel mutated in the disease cystic fibrosis, plays an essential role in duodenal bicarbonate secretion. Our data are consistent with the hypothesis that cellular bicarbonate loading is an important means of preserving epithelial pHi during luminal acid challenge. Increased MGT may damp rapid shifts of luminal pH. Enhanced mucosal blood flow plays a significant role in the removal of back-diffusing acid. These neurally coordinated systems act coherently to defend the vulnerable duodenal epithelial cells from concentrated gastric acid.

5

Muscarinic acetylcholine receptor subtype 4 is esssential for cholinergic stimulation of duodenal bicarbonate secretion in mice - relationship to D cell/somatostatin

80%

Takeuchi K., Kita K., Takahashi K., Aihara E., Hayashi S.

Journal of Physiology and Pharmacology

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2015

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tom 66

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nr 3

6

Duodenal mucosal protection by bicarbonate secretion and its mechanisms

80%

Konturek S. J., Konturek P. C., Pawlik T., Sliwowski Z., Ochmanski W., Hahn E. G.

Journal of Physiology and Pharmacology. Supplement

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2004

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tom 55

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nr 2

5-17

Proximal portion of duodenum is exposed to intermittent pulses of gastric H+ discharged by the stomach. This review summarizes the mechanisms of duodenal mucosal integrity, mainly the role of mucus-alkaline secretion and the mucous barrier protecting surface epithelium against gastric H+. The mucous barrier protects the leaky duodenal epithelium against each pulse of gastric H+, which penetrates this barrier and diffuses into duodenocytes, but fails to damage them due to; a) an enhanced expression of cyclooxygenase-1 (COX-1), with release of protective prostaglandins (PG) and of nitric oxide (NO) synthase (NOS) with, however, production of NO, stimulating duodenal HCO3- secretion and b) the release of several neurotransmitters also stimulating HCO3- secretion such as vasoactive intestimal peptide (VIP), pituitary adenylate-cyclase activating polypeptide (PACAP), acetylcholine, melatonin, leptin and ghrelin released by enteric nerves and mucosal cells. At the apical duodenocyte membrane at least two HCO3-/Cl- anion exchangers operate in response to luminal H+ to provide adequate extrusion of HCO3- into duodenal lumen. In the basolateral portion of duodenocyte membrane, both non-electrogenic (NBC) and electrogenic (NBCn) Na+-HCO3- cotransporters are activated by the exposure to duodenal acidification, causing inward movement of HCO3- from extracellular fluid to duodenocytes. There are also at least three Na+/H+ (NHE1-3) amiloride-sensitive exchangers, eliminating H+ which diffused into these cells. The Helicobacter pylori (Hp) infection and gastric metaplasia in the duodenum with bacterium inoculating metaplastic mucosa and inhibiting HCO3- secretion by its endogenous inhibitor, asymetric dimethyl arginine (ADMA), may result in duodenal ulcerogenesis.

7

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Suppression of Helicobacter pylori protease activity towards growth factors by sulglycotide

80%

Piotrowski J., Slomiany A., Slomiany B. L.

Journal of Physiology and Pharmacology

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1997

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tom 48

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nr 3

Ograniczanie wyników

Neurally-mediated and neurally-independent beneficial actions of melatonin in the gastrointestinal tract

Central nervous stimuli increase duodenal bicarbonate secretion by release of mucosal melatonin

Vectorial bicarbonate transport by Par-C10 salivary cells

Acid-sensing protective mechanisms of duodenum

Muscarinic acetylcholine receptor subtype 4 is esssential for cholinergic stimulation of duodenal bicarbonate secretion in mice - relationship to D cell/somatostatin

Duodenal mucosal protection by bicarbonate secretion and its mechanisms

Suppression of Helicobacter pylori protease activity towards growth factors by sulglycotide