Effect of intracerebroventricular administration of thyrotropin-releasing hormone upon the electroenteromyogram of rat duodenum

Tonoue, Teiichiro; Nomoto, Teruko

doi:10.1016/0014-2999(79)90307-8

Cited by 39 publications

(3 citation statements)

References 19 publications

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“…Definite proof of such a role of TRH, however, will depend on the demonstration that a specific TRH antagonist or antiserum affects intestinal peristalsis. As intracerebrally administered TRH also markedly influences gastrointestinal motor activity (21)(22)(23) it appears that TRH may regulate gastrointestinal motility at both a central and a local enteric level.…”

Section: Discussionmentioning

confidence: 99%

Thyrotropin‐Releasing Hormone Potently Modulates Peristaltic Motor Activity of the Guinea Pig Small Intestine

Holzer

Pertl

Wolf

1989

Neurogastroenterology Motil

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Thyrotropin‐releasing hormone (TRH) is present in enteric neurons of the guinea pig intestine, which indicates it may have a role in the control of gut motility. Isolated segments of the guinea pig duodenum‐jejunum and ileum were used to examine the effect of TRH on intestinal peristalsis. The peristaltic waves in the proximal small intestine were triggered at a higher intraluminal pressure and exhibited a higher frequency and a lower amplitude than those in the ileum. TRH (0.3–300 nM) induced a concentration‐related increase in the pressure threshold at which peristaltic waves were elicited and a moderate decrease in the amplitude of the peristaltic waves in both regions. However, while the frequency of the peristaltic waves was increased by the peptide in the ileum, it was diminished by TRH (0.3 and 3 nM) in the duodenum‐jejunum. Since the contractile effect of carbachol on the circular muscle of the duodenum‐jejunum remained unaffected by TRH, it appears that the peptide does not act on the muscle directly but influences peristalsis by acting on enteric neurons. The data further suggest that TRH released from enteric neurons may play a physiologic role in the regulation of propulsive motor activity of the gut.

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Section: Discussionmentioning

confidence: 99%

Thyrotropin‐Releasing Hormone Potently Modulates Peristaltic Motor Activity of the Guinea Pig Small Intestine

Holzer

Pertl

Wolf

1989

Neurogastroenterology Motil

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“…The high doses of atropine (1 or 10 mg kg-1) did not prevent indomethacin ulcers (Watanabe, Watanabe, Maeda-Magiwara & Kanaoka, 1983;Bates, Buckley & Strettle, 1981). It has been demonstrated that TRH acts in the CNS to influence profoundly the muscular activity of the gut Smith et al, 1977;Tonoue & Nomoto, 1979;Horita & Carino, 1982;LaHann & Horita, 1982). William & Hinchey (1981) reported a synergism between acid and the gastric contractile activity in the genesis of ulceration of phenylbutazonetreated rats.…”

Section: Discussionmentioning

confidence: 99%

“…It has become evident that TRH influences the gastrointestinal tract in animals and man in many ways (Morley, 1979;Jackson, 1982). One of the recently described properties of centrally administered TRH is its ability to increase the motor activity of the gastrointestinal tract Smith, LaHann, Chestnut, Carino & Horita, 1977;Tonoue & Nomoto, 1979;Horita & Carino, 1982;LaHann & Horita, 1982). Although a considerable amount of work has been conducted on TRH-induced gastric acid secretion (Tache, Vale & Brown, 1980;Morley, Levine & Silvis, 1981; Maeda-Hagiwara & Watanabe, 1983a), there are few studies about the influence of TRH on the gastric mucosa (Tache, Simard & Collu, 1979).…”

Section: Introductionmentioning

confidence: 99%

Enhancement by intracerebroventricular thyrotropin‐releasing hormone of indomethacin‐induced gastric lesions in the rat

Maeda-Hagiwara

Watanabe

1983

British J Pharmacology

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1Effects of the intracerebroventricular thyrotropin-releasing hormone (TRH) on gastric mucosa were studied in rats. 2 TRH (3 and 10 lAg ratr 1 i.c.v.) produced slight gastric lesions and also aggravated indomethacin-, aspirin-or 5-hydroxytryptamine (5-HT)-induced gastric lesions, while restraint and cold stressinduced lesions were not influenced by TRH. 3 Bethanechol used at a dose sufficient to produce acid secretion did not influence the gastric mucosa in intact or indomethacin-treated rats. 4 Enhancement of indomethacin-induced gastric lesions by TRH was not inhibited to any significant degree by atropine 0.1 mg kg-I s.c., which prevented TRH-induced gastric acid secretion, but tended to be inhibited by phentolamine, 2.5 mg kg-1 i.p. 5It is concluded that the enhancement by TRH of indomethacin-induced gastric lesions is due to a combination of the central and peripheral actions of the ulcerogenic agents.

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TRH Interactions with Cholinergic Mechanisms and Consequent Therapeutic Implications

Yarbrough

1984

Psychoneuroendocrine Dysfunction

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Effect of intracerebroventricular administration of thyrotropin-releasing hormone upon the electroenteromyogram of rat duodenum

Cited by 39 publications

References 19 publications

Thyrotropin‐Releasing Hormone Potently Modulates Peristaltic Motor Activity of the Guinea Pig Small Intestine

Thyrotropin‐Releasing Hormone Potently Modulates Peristaltic Motor Activity of the Guinea Pig Small Intestine

Enhancement by intracerebroventricular thyrotropin‐releasing hormone of indomethacin‐induced gastric lesions in the rat

TRH Interactions with Cholinergic Mechanisms and Consequent Therapeutic Implications

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