Dual action of clonidine on ethanol-induced gastric lesions: is the imidazoline-preferring receptor involved?

Bhandare, Padma N.; Rataboli, Padmanabh V.; D'Souza, R S

doi:10.1016/0014-2999(91)90464-2

Cited by 20 publications

(8 citation statements)

References 12 publications

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“…Nevertheless, α 2 -adrenoceptor antagonism significantly increased the severity of 100% ethanol-induced mucosal injury and completely blocked the cytoprotective action of 20% ethanol, although the effects of 5% NaCl and 0.3 M HCl were not affected. This result was supported by the report that α 2 -adrenoceptor agonists clonidine and α-methyldopa possessed gastroprotective effects [18]. Blocking the α 2 -adrenoceptors would prevent the negative feedback action on the release of catecholamines from presynaptic nerve terminals, which could participate at least partly in the adaptive cytoprotection of 20% ethanol and the mucosal defensive mechanisms of the stomach in general.…”

Section: Involvement Of Different Components Of the Autonomic Nervoussupporting

confidence: 74%

Adaptive Cytoprotection and the Brain-Gut Axis

Cho

2011

Digestion

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Adaptive cytoprotection is a concept to counteract against the gastric mucosal injury caused by stress, strong irritants and drugs such as non-steroidal anti-inflammatory drugs. The process is mediated through diverse mediators and mechanisms. Studies on adaptive cytoprotection began from the discovery of prostaglandin (PG)-dependent and PG-independent pathways, followed by the investigation on the types and concentrations of mild irritants to be used. Upon the confirmation on the importance of the vagus nerve and the vago-vagal pathway in regulating the mucosal protective actions of the mild irritants, individual participating mediators for the neuronal modulatory processes were explored, including peptide neurotransmitters such as calcitonin gene-related peptide and substance P. Further correlation with the sympathetic nervous system, the sensory afferent neurons and the enteric nervous system of the gastric mucosa had been made. A close working relationship between the hypothalamic-pituitary-adrenal axis, the autonomic nervous system and the enteric nervous system was then proposed, with concurrent regulation of PG, nitric oxide and sensory neuropeptides by different mild irritants. Apart from these conventional concepts, there are now contemporary ideas on newer forms of adaptive cytoprotection such as ischemic preconditioning and heat-shock proteins, which will cast new light to novel approaches in facilitating gastric mucosal protection.

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Section: Involvement Of Different Components Of the Autonomic Nervoussupporting

confidence: 74%

Adaptive Cytoprotection and the Brain-Gut Axis

Cho

2011

Digestion

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Section: Functional Experimentsmentioning

confidence: 99%

“…It has also been speculated that stimulation of gastric acid release induced by high concentrations of clonidine and related compounds in rat and guinea pig, 25–28 might be due to activation of imidazoline receptors. 1,27 The putative endogenous ligand at imidazoline sites, agmatine, 29 resembled the other guanidine and imidazoline derivatives in that it increased gastric acid secretion after systemic application. 28 To investigate whether imidazoline derivatives increase acid secretion by direct activation of the gastric glands, we used [ 14 C]aminopyrine accumulation in isolated rabbit gastric glands (the standard in vitro method for this purpose) as a model for the study of acid secretory mechanisms of the mammalian parietal cells.…”

Section: Functional Experimentsmentioning

confidence: 99%

Imidazoline Recognition Sites and Stomach Function^a

Molderings

Burian

Menzel

et al. 1999

Annals of the New York Academy of Sciences

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Radioligand binding experiments carried out in cell membranes from rat and human stomach revealed the existence of non-adrenoceptor [3H]clonidine and [3H]idazoxan binding sites and of [3H]DTG (1,2-di-(2-tolyl)guanidine) binding sites. In rat stomach, specific binding was inhibited by imidazolines and guanidines and by non-imidazoline sigma-site ligands, respectively, at different rank orders of affinity, suggesting the existence of non-I1/non-I2 [3H]clonidine binding sites, I2-imidazoline binding sites as well as sigma 2-like-sites. These sites are not directly related to a postsynaptic contractile effect on rat gastric smooth muscle or to acid release from isolated gastric glands. Finally, we demonstrated that the gastric pathogen Helicobacter pylori is able to form and to release the endogenous imidazoline receptor ligand agmatine and that considerable amounts of agmatine are present in human gastric juice. The quantities of agmatine were higher in gastric juice from H. pylori-positive than H. pylori-negative patients.

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“…In this context, five findings are worth being noted: (1) In the rat clonidine 0.1 mg/kg given i.p. was shown to protect against ethanol-induced gastric lesions (presumably via activation of α 2 -adrenoceptors), while the same dose given orally had an aggravating effect (Bhandare et al 1991). (2) The stomach represents the tissue with the highest content of agmatine in mammalian organisms (Raasch et al 1995).…”

Section: Resultsmentioning

confidence: 99%

Imidazoline derivatives and agmatine induce histamine release from the rat stomach

Molderings

Menzel

Göthert

1999

Naunyn-Schmiedeberg's Arch Pharmacol

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Strips from rat glandular stomach were used to investigate whether the imidazoline derivatives clonidine, tolazoline and BDF 6143 (4-chloro-2(2-imidazolin-2-ylamino)-isoindoline) and the guanidine derivative agmatine are able to release histamine from histamine-storing cells. Histamine was detected and quantified by HPLC. Clonidine, tolazoline and agmatine concentration-dependently induced a release of histamine from the gastric strips, whereas BDF 6143 was ineffective. However, BDF 6143 abolished the release-inducing effect of clonidine and agmatine. It is concluded that imidazoline and guanidine derivatives can induce histamine release from histamine-storing cells in the stomach by a specific mechanism (possibly via imidazoline receptors) which in turn might lead to a relevant increase in gastric acid secretion.

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Dual action of clonidine on ethanol-induced gastric lesions: is the imidazoline-preferring receptor involved?

Cited by 20 publications

References 12 publications

Adaptive Cytoprotection and the Brain-Gut Axis

Adaptive Cytoprotection and the Brain-Gut Axis

Imidazoline Recognition Sites and Stomach Function^a

Imidazoline derivatives and agmatine induce histamine release from the rat stomach

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Dual action of clonidine on ethanol-induced gastric lesions: is the imidazoline-preferring receptor involved?

Cited by 20 publications

References 12 publications

Adaptive Cytoprotection and the Brain-Gut Axis

Adaptive Cytoprotection and the Brain-Gut Axis

Imidazoline Recognition Sites and Stomach Functiona

Imidazoline derivatives and agmatine induce histamine release from the rat stomach

Contact Info

Product

Resources

About

Imidazoline Recognition Sites and Stomach Function^a