Gastric distension‐induced pyloric relaxation: central nervous system regulation and effects of acute hyperglycaemia in the rat

Ishiguchi, Tadashi; Nakajima, Mitsutoshi; Sone, Hirohito; Tada, Hitoshi; Kumagai, Arno K.; Takahashi, Toshio

doi:10.1111/j.1469-7793.2001.t01-1-00801.x

Cited by 40 publications

(44 citation statements)

References 43 publications

(66 reference statements)

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“…Animal studies demonstrate pyloric relaxation induced by gastric distension is significantly reduced by subdiaphragmatic vagotomy, thereby prohibiting food passage [24]. Furthermore, demyelinating disease in the medullary region of the brainstem, presumably the vagal nerve nuclei, secondary to multiple sclerosis, has been correlated with gastroparesis and abnormal gastric emptying studies [25].…”

Section: Gut Pathophysiologymentioning

confidence: 98%

What the Gut Can Teach Us About Migraine

Hindiyeh

Aurora

2015

Curr Pain Headache Rep

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During gestation, cells of the brain and gut develop almost simultaneously into the central nervous system (CNS) and enteric nervous system (ENS), respectively. They remain connected via the vagal nerve lifelong. While it is well known that the brain sends signal to the gut, communication is in fact bidirectional. Just as the brain can modulate gut functioning, the gut, and likely what we ingest, can in fact influence our brain functioning. We will first review both gastrointestinal (GI) function and migraine pathophysiology and then discuss evidence linking the migraine brain to various GI disorders. Lastly, we discuss the effects of gut microbiota on brain functioning and speculate how the gut and particularly diet may affect migraine.

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Section: Gut Pathophysiologymentioning

confidence: 98%

What the Gut Can Teach Us About Migraine

Hindiyeh

Aurora

2015

Curr Pain Headache Rep

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“…Gastric distension-induced pyloric relaxation is significantly reduced by subdiaphragmatic vagotomy, hexamethonium, and l-NAME, but not by splanchnicotomy and guanethidine. 53 This suggests that gastric distension-induced pyloric relaxation is mediated via the vagus and NO neurons.…”

Section: Pyloric Sphinctermentioning

confidence: 99%

Pathophysiological significance of neuronal nitric oxide synthase in the gastrointestinal tract

Takahashi

2003

Journal of Gastroenterology

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242

181

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It has been demonstrated that nitric oxide (NO) is a major inhibitory nonadrenergic, noncholinergic (NANC) neurotransmitter in the gastrointestinal (GI) tract. NO released in response to nerve stimulation of the myenteric plexus causes relaxation of the smooth muscle. NO is synthesized by the activation of neuronal NO synthase (nNOS) in the myenteric plexus. Released NO plays an important physiological role in various parts of the GI tract. NO regulates the muscle tone of the sphincter in the lower esophagus, pylorus, sphincter of Oddi, and anus. NO also regulates the accommodation reflex of the fundus and the peristaltic reflex of the intestine. Previous studies have shown that NOS inhibitors delay gastric emptying and colonic transit. The reduction of nNOS expression, associated with impaired local production of NO, may be responsible for motility disorders in the GI tract. There is accumulated evidence that dysfunction of NO neurons in the myenteric plexus may cause various GI diseases. These reports are reviewed and possible mechanisms of altered nNOS expression are discussed in this article. In particular, impaired nNOS synthesis of the myenteric plexus seems to be an important contributing factor to the pathogenesis of achalasia, diabetic gastroparesis, infantile hypertrophic pyloric stenosis, Hirschsprung's disease, and Chagas' disease. Reduced NO release and/or nNOS expression are suspicious in a subset of patients with functional dyspepsia. Although the etiology of intestinal pseudo-obstruction remains unknown, it is conceivable that extrinsic denervation may upregulate nNOS expression, resulting in enhanced muscular relaxation and disturbed peristalsis. An animal model of colitis showed impaired nNOS expression in the colonic myenteric plexus. Antecedent infection may be associated with the impaired NO pathways observed in functional dyspepsia, colitis, and Chagas' disease.

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“…It has been reported that metabolites of L-arginine mediate neuronal inhibition of canine pyloric motor activity in vivo (Allescher et al, 1992) and facilitate gastric emptying by inhibiting pyloric contractions (Orihata and Sarna, 1994). Gastric distension-induced pyloric relaxation appears to be mediated via a vago-vagal reflex and NO release in the rat (Ishiguchi et al, 2001). The primary site of action of nitrergic mechanisms on the gastric fundic tone in conscious dogs is likely to be at a presynaptic level on the vagal cholinergic efferent nerves (Paterson et al, 2000).…”

mentioning

confidence: 99%