Inhibitory neural pathway regulating gastric emptying in rats

Ishiguchi, Tadashi; Nishioka, Satoshi; Takahashi, Toshio

doi:10.1016/s0165-1838(99)00103-4

Cited by 22 publications

(21 citation statements)

References 22 publications

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“…Consistent with these results, the radiographs showed that tacrine, applied in the dosage we used, partially inhibited peristaltic activity and even caused hypotonia in parts of the stomach and cecum. These effects, as well as the lack of stenotic areas along the tract (observed in prolonged ingestion of other cholinesterase inhibitors [22,23] ), distinguish the overall tacrine action on the GI tract that we observed. The overall tacrine action cannot be immediately connected with its anticholinesterase action, since ACh, accumulated in GI tract tissues, usually depolarizes SM tissues [24] , increases contractile activity [24,25] and tone [26] , and accelerates intestinal passage.…”

Section: Discussionsupporting

confidence: 52%

“…Resistance additionally increased as a result of the increased reactivity of SM from both areas mentioned, brought about by ACh, the concentration of which increased in the tissues following each intake of the drug. All this hindered CM passage, and it is well known that pyloric relaxation is accepted to be the most important factor for gastric evacuation [22] .…”

Section: Discussionmentioning

confidence: 99%

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Delayed Evacuatory Function due to Specific Smooth Muscle Reactivity in the Gastrointestinal Tracts of Tacrine-Treated Rats

Krustev

Sirakov²,

Turiiski³

et al. 2007

Pharmacology

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Most of the side effects induced by tacrine are associated with the gastrointestinal (GI) tract. The aim of the study was to analyze the nature of radiographically registered, tacrine-induced changes in evacuatory function, as well as to find a possible correlation with the immediate in vitro action of the drug on smooth muscles from the GI tracts of rats. The tacrine dose we used reliably delayed GI passage: contrast matter was not fully evacuated, predominantly from the stomach and cecum. The delay resulted from changes in tone and peristaltic activity, specific for the various regions of the tract. These changes were associated with a superposing of the responses due to the anticholinesterase and noncholinergic action of tacrine.

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Section: Discussionsupporting

confidence: 52%

Section: Discussionmentioning

confidence: 99%

Delayed Evacuatory Function due to Specific Smooth Muscle Reactivity in the Gastrointestinal Tracts of Tacrine-Treated Rats

Krustev

Sirakov²,

Turiiski³

et al. 2007

Pharmacology

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“…PACAP was reported to be involved in regulation of motility of the porcine antrum [40]. PACAP was also reported to relax the rat pyloric sphincter [19]. PACAP-immunoreactive fibers and nerve cell bodies were found in the myenteric ganglia of the stomach including antrum [15,30,37].…”

Section: Discussionmentioning

confidence: 95%

Roles of PACAP and PHI as inhibitory neurotransmitters in the circular muscle of mouse antrum

Toyoshima

Takeuchi

Goto

et al. 2005

Pflugers Arch - Eur J Physiol

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Mediators of neurogenic responses of the gastric antrum were studied in wild-type and pituitary adenylate cyclase-activating polypeptide (PACAP) -knockout (KO) mice. Electrical field stimulation (EFS) to the circular muscle strips of the wild-type mouse antrum induced a triphasic response; rapid transient relaxation and contraction, and sustained relaxation that was prolonged for an extended period after the end of EFS. The transient relaxation and contraction were completely inhibited by L-nitroarginine and atropine, respectively. The sustained relaxation was significantly inhibited by a PACAP receptor antagonist, PACAP(6-38). The antral strips prepared from PACAP-KO mice unexpectedly exhibited a tri-phasic response. However, the sustained relaxation was decreased to about one-half of that observed in wild-type mice. PACAP(6-38) inhibited EFS-induced sustained relaxation (33.5% of control) in PACAP-KO mice. Anti-peptide histidine isoleucine (PHI) serum partially (the 30% inhibition) or significantly (the 60% inhibition) inhibited the sustained relaxations in the wild-type and PACAP-KO mice, respectively. The immunoreactivities to the anti-PACAP and anti-PHI serums were found in myenteric ganglia of the mouse antrum. These results suggest that nitric oxide and acetylcholine mediate the transient relaxation and contraction, respectively, and that PACAP and PHI separately mediate the sustained relaxation in the antrum of the mouse stomach.

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“…We have previously shown that hexamethonium (20 mg kg _1 ) and L-NAME (10 mg kg _1 ) inhibited vagally stimulated pyloric motor responses (Ishiguchi et al 2000a). We have also shown that guanethidine (5 mg kg _1 ) significantly inhibited CCK 8-induced gastric relaxation (Takahashi & Owyang, 1999).…”

Section: Effects Of Various Neural Blocking Agentsmentioning

confidence: 94%

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

Ishiguchi

Nakajima

Sone

et al. 2001

The Journal of Physiology

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Pyloric sphincter tone plays an important role in the regulation of gastric emptying. Non-adrenergic, noncholinergic (NANC) innervation to the pylorus is predominantly inhibitory and mediates relaxation of the sphincter (Anuras et al. 1974). A high density of NOSimmunopositive nerve cells and fibres has been demonstrated in the pylorus (Ekblad et al. 1994), and significant reduction of NOS activity of the pylorus has been demonstrated in infantile hypertrophic pyloric stenosis (Vanderwinden et al. 1992). It has been shown that transgenic mice with homozygous depletion of the nNOS gene develop grossly enlarged stomachs with hypertrophy of the pyloric sphincter (Huang et al. 1993). Thus, gastric outlet obstruction is associated with the lack of NO-generating neurons in the pylorus. Previous studies have shown that NO biosynthesis inhibitors delay Gastric distension-induced pyloric relaxation: central nervous system regulation and effects of acute hyperglycaemia in the rat 1. The pylorus plays an important role in the regulation of gastric emptying. In addition to the autonomic neuropathy associated with long-standing diabetes, acute hyperglycaemia per se has effects on gastric emptying. In this study, the role of the central nervous system in modulating the effects of hyperglycaemia on gastric distension-induced pyloric relaxation was investigated.2. Gastric distension-induced pyloric relaxation was significantly reduced by subdiaphragmatic vagotomy, hexamethonium (20 mg kg _1 ) and N G -nitro-L-arginine methyl ester (L-NAME; 10 mg kg _1 ), a nitric oxide synthase (NOS) biosynthesis inhibitor, in anaesthetized rats. In contrast, neither splanchnectomy nor guanethidine (5 mg kg _1 ) had an effect. 8. Taken together, these findings suggest that gastric distension-induced pyloric relaxation is mediated via a vago-vagal reflex and NO release. Acute hyperglycaemia stimulates hypothalamic NPY release, which, acting through the Y1 receptor, inhibits gastric distensioninduced pyloric relaxation in rats exposed to acute elevations in blood glucose concentrations.

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Inhibitory neural pathway regulating gastric emptying in rats

Cited by 22 publications

References 22 publications

Delayed Evacuatory Function due to Specific Smooth Muscle Reactivity in the Gastrointestinal Tracts of Tacrine-Treated Rats

Delayed Evacuatory Function due to Specific Smooth Muscle Reactivity in the Gastrointestinal Tracts of Tacrine-Treated Rats

Roles of PACAP and PHI as inhibitory neurotransmitters in the circular muscle of mouse antrum

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

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