The role of calcitonin gene‐related peptide in gastric mucosal protection in the rat

Forster, E.R.; Dockray, G. J.

doi:10.1113/expphysiol.1991.sp003532

Cited by 21 publications

(6 citation statements)

References 5 publications

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“…RX 77368-induccd gastric protection against 60% ethanol. These results are consistent with the well-established gastric protective ac tion against damaging agents induced by CGRP either exogenously administered or endogenously released by acute gastric perfusion with capsaicin [8,[40][41][42], Conver gent pharmacological, functional and anatomical studies indicate that the protective effect of CGRP against etha nol is primarily related to the nitric oxide dependent and PGs independent increase in gastric mucosal blood (low [8,40]. In the present study it is likely CGRP protective action is mediated through similar mechanisms.…”

Section: Discussionsupporting

confidence: 79%

Role of Prostaglandins and Calcitonin Gene-Related Peptide in Central Vagal Cholinergic-Dependent Protection against Gastric Injury in Urethane-Anesthetized Rats

Kato¹,

Yang²,

Taché³

1996

Digestion

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The influence of central vagal activation induced by the thyrotropin-releasing hormone (TRH) analog, RX 77368, injected intracisternally on gastric mucosal injury produced by 60% ethanol (4 ml·kg^-1) was investigated in urethane-anesthetized rats. RX 77368 (3, 10 and 30 ng) inhibits dose dependently macroscopic gastric damage induced by intragastric administration of 60% ethanol by 18,43 and 77%, respectively. The cytoprotective effect of intracisternal RX 77368 (30 ng) was completely blocked by cervical vagotomy, atropine (2 mg·kg^-1 s.c), and CGRP_8-37 (100 μg·kg^-1 i.v.) and partially inhibited by indomethacin (5mg·kg-¹ i.p.). Vagotomy, atropine, indomethacin and CGRP8-37 alone did not modify gastric mucosal lesions induced by ethanol in rats injected intracisternally with saline. The present data show that intracisternal injection of TRH analog in urethane-anesthetized rats protects against ethanol-induced gastric injury through vagal cholinergic dependent pathways which recruit prostaglandins and CGRP mechanisms.

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Section: Discussionsupporting

confidence: 79%

Role of Prostaglandins and Calcitonin Gene-Related Peptide in Central Vagal Cholinergic-Dependent Protection against Gastric Injury in Urethane-Anesthetized Rats

Kato¹,

Yang²,

Taché³

1996

Digestion

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“…Chemical irritants caused release of CGRP (Gepetti et al, 1991), and reduced gastric CGRP concentration (Evangelista et al, 1993). Close arterial infusion of CGRP inhibited irritant-induced hemmorragic damage (Lippe et al, 1989), and CGRP immunoneutralization enhanced irritant-induced damage (Forster and Dockray, 1991;Holzer, 1998). Recently Kang et al (1998) provided evidence of a cross-talk between EGF and capsaicin sensitive nerves during ulcer healing.…”

Section: Neuromessengers and Ulcer Healingmentioning

confidence: 99%

Innervation of the gastric mucosa

Ekblad

Mei

Sundler

2000

Microsc. Res. Tech.

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A plethora of neuronal messengers (“classical” transmitters, gaseous messengers, amino acid transmitters, and neuropeptides) are capable of mediating or modulating gastric functions. Accordingly, the stomach is richly innervated. Gastric nerves are either intrinsic to the gastric wall, i.e., they have their cell bodies in the intramural ganglia and thus belong to the enteric nervous system, or they reach the stomach from outside, originating in the brainstem, in sympathetic ganglia, or in sensory ganglia. Topographically, the nerve fibers in the stomach reach all layers from the most superficial portions of the gastric glands to the outer smooth muscle layer. This wide distribution implies that virtually all different cell types may be reached by neuronal messengers. Within the gastric mucosa endocrine and paracrine cells (e.g., gastrin cells, ECL cells, somatostatin cells), exocrine cells (parietal cells, chief cells, mucous cells), smooth muscle cells, and stromal cells are regulated by neuronal messengers. The sensory innervation, responding to capsaicin, plays an important role in mucosal protection, and in ulcer healing. Presumably also other nerves are involved and a plasticity in the neuropeptide expression has been demonstrated at the margin of gastric ulcers. Taken together, available data indicate a complex interplay between hormones, paracrine messengers and neuronal messengers, growth factors and cytokines in the regulation of gastric mucosal activities such as secretion, local blood flow, growth, and restitution after damage. Microsc. Res. Tech. 48:241–257, 2000 © 2000 Wiley‐Liss, Inc.

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“…Thereafter animals were taken for experiments as described below. The presence of circulating CGRP antibodies was verified by incubation of plasma in serial dilutions with 125I-labeled rat Tyro otCGRP28-37 as previously described ( 15,21,22).…”

Section: Methodsmentioning

confidence: 99%

“…The protocol used to generate neutralizing antibodies has previously been described (21 ). In brief, experimental animals were induced to produce their own antibody by immunization with rat Tyro aCGRP28-37 conjugated to thyroglobulin by glutaraldehyde as described previously (21 ).…”

Section: Methodsmentioning

confidence: 99%

Differential control of somatostatin messenger RNA in rat gastric corpus and antrum. Role of acid, food, and capsaicin-sensitive afferent neurons.

Sandvik

Dimaline²,

Forster³

et al. 1993

J. Clin. Invest.

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Somatostatin messenger RNA in the antrum and corpus of rat stomach was quantified by Northern and slot blotting using a probe generated by the polymerase chain reaction. Fasting for 48 h enhanced the abundance of somatostatin mRNA in the pyloric antral region, but not in the acid-secreting region of the stomach. In fasted rats, somatostatin mRNA in antrum, but not corpus, was decreased by inhibition of acid secretion with omeprazole. In contrast, in rats treated with capsaicin to lesion small diameter afferents there was a significant decrease in somatostatin mRNA abundance in the corpus but not antrum. The effects of capsaicin cannot be attributed to nonspecific changes in gastric endocrine cell gene expression, since the abundance of histidine decarboxylase mRNA (which is a functionally regulated marker for a different gastric endocrine cell type) did not change with capsaicin. Gastric capsaicin-sensitive afferents are rich in calcitonin gene-related peptide, and in rats with antibodies to this peptide there was reduced corpus somatostatin mRNA. Moreover, infusion of calcitonin gene-related peptide in control rats produced a significant increase in somatostatin mRNA in the gastric corpus. The results indicate that somatostatin mRNA abundance is controlled by the gastric luminal contents and the extrinsic afferent innervation, but the relative importance of these factors differs in antrum and corpus: luminal contents are relatively more important in antrum and primary afferents using calcitonin gene-related peptide in the corpus. (J. Clin. Invest. 1993. 91:244-250.)

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The role of calcitonin gene‐related peptide in gastric mucosal protection in the rat

Cited by 21 publications

References 5 publications

Role of Prostaglandins and Calcitonin Gene-Related Peptide in Central Vagal Cholinergic-Dependent Protection against Gastric Injury in Urethane-Anesthetized Rats

Role of Prostaglandins and Calcitonin Gene-Related Peptide in Central Vagal Cholinergic-Dependent Protection against Gastric Injury in Urethane-Anesthetized Rats

Innervation of the gastric mucosa

Differential control of somatostatin messenger RNA in rat gastric corpus and antrum. Role of acid, food, and capsaicin-sensitive afferent neurons.

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