Intracerebral adrenoceptor agonists influence rat duodenal mucosal bicarbonate secretion

Larson, Gerald M.; Jedstedt, Gunilla; Nylander, Olof; Flemström, Gunnar

doi:10.1152/ajpgi.1996.271.5.g831

Cited by 13 publications

(27 citation statements)

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“…Bilateral cutting of the vagal trunks at the sublaryngeal level inhibits the stimulation of duodenal (6, 7) and pancreatic (29) secretion induced by intracerebroventricular infusion of the neuropeptide TRH. Truncal vagotomy alone also abolishes the responses to intracerebroventricular administration of bombesin (6) and intracerebroventricular or intravenous administration of some benzodiazepines (9), but identical vagotomy does not affect the response to intracerebroventricular phenylephrine (5). It was found in the present study that cutting all nerves around the carotid arteries, in contrast to sympathectomy alone and findings after truncal vagotomy, markedly inhibits the duodenal secretory response to intracerebroventricular phenylephrine (Figure 4).…”

Section: Discussionmentioning

confidence: 53%

“…Bilateral cutting of the vagal trunks inhibits the rise in duodenal secretion induced by intracerebroventricular infusion of TRH and some other agents (6,7,9), but the same kind of vagotomy (at the sublaryngeal level) does not affect the response to intracerebroventricular phenylephrine (5). Effects of extended pericarotid nervectomies were tested in the present study ( Figure 4).…”

Section: Resultsmentioning

confidence: 87%

“…Intracerebroventricular infusion of the α 1 -selective adrenoceptor agonist phenylephrine causes marked stimulation of duodenal HCO 3 -secretion in the rat (5). This rise in secretion is inhibited by the ganglion blocking agent hexamethonium and by central nervous (but not by intravenous) administration of the adrenoceptor antagonist prazosin.…”

Section: Introductionmentioning

confidence: 96%

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Peripheral melatonin mediates neural stimulation of duodenal mucosal bicarbonate secretion

Sjöblom¹,

Jedstedt²,

Flemström³

2001

J. Clin. Invest.

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Melatonin is released from intestinal enterochromaffin cells and from the pineal gland, but its role in gastrointestinal function is largely unknown. Our aim was to study the involvement of intestinal and central nervous melatonin in the neurohumoral control of the duodenal mucosa-protective bicarbonate secretion. Working in anesthetized rats, we cannulated a 12-mm segment of duodenum with an intact blood supply and titrated the local bicarbonate secretion with pH-stat. Melatonin and receptor ligands were supplied to the duodenum by close intra-arterial infusion. Even at low doses, melatonin and the full agonist 2-iodo-N-butanoyl-5-methoxytryptamine increased duodenal bicarbonate secretion. Responses were inhibited by the predominantly MT 2 -selective antagonist luzindole but not by prazosin, acting at MT 3 receptors. Also, luzindole almost abolished the marked rise in secretion induced by intracerebroventricular infusion of the adrenoceptor agonist phenylephrine. This response was also abolished by sublaryngeal ligation of all nerves around the carotid arteries. However, it was insensitive to truncal vagotomy alone or sympathectomy alone and was unaffected by removal of either the pineal gland or pituitary gland. Thus, melatonin stimulates duodenal bicarbonate secretion via action at enterocyte MT 2 -receptors and mediates neural stimulation of the secretion.

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Section: Discussionmentioning

confidence: 53%

Section: Resultsmentioning

confidence: 87%

Section: Introductionmentioning

confidence: 96%

See 1 more Smart Citation

Peripheral melatonin mediates neural stimulation of duodenal mucosal bicarbonate secretion

Sjöblom¹,

Jedstedt²,

Flemström³

2001

J. Clin. Invest.

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“…It should also be noted that the hepatic branch that enters the duodenum via the perivascular plexuses of the hepatic, gastroduodenal, and superior pancreaticoduodenal arteries innervates primarily the duodenum. Previous studies with the present type of in situ chamber preparation have shown that intracerebroventricular administration of the peptide hormone TRH (16,30) or the catecholamine phenylephrine (28,44) induces vagally mediated stimulation of duodenal alkaline secretion. Furthermore, it has been shown that electrical stimulation of the cut cervical vagal nerves in the distal direction does stimulate the secretion in rat and also cat duodenum in situ (22,36).…”

Section: Discussionmentioning

confidence: 61%

Food-induced expression of orexin receptors in rat duodenal mucosa regulates the bicarbonate secretory response to orexin-A

Bengtsson

Mäkelä²,

Sjöblom³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

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Presence of appetite-regulating peptides orexin-A and orexin-B in mucosal endocrine cells suggests a role in physiological control of the intestine. Our aim was to characterize orexin-induced stimulation of duodenal bicarbonate secretion and modulation of secretory responses and mucosal orexin receptors by overnight food deprivation. Lewis x Dark Agouti rats were anesthetized and proximal duodenum cannulated in situ. Mucosal bicarbonate secretion (pH stat) and mean arterial blood pressure were continuously recorded. Orexin-A was administered intra-arterially close to the duodenum, intraluminally, or into the brain ventricles. Total RNA was extracted from mucosal specimens, reverse transcribed to cDNA and expression of orexin receptors 1 and 2 (OX1 and OX2) measured by quantitative real-time PCR. OX1 protein was measured by Western blot. Intra-arterial orexin-A (60-600 nmol.h(-1).kg(-1)) increased (P < 0.01) the duodenal secretion in fed but not in fasted animals. The OX1 receptor antagonist SB-334867, which was also found to have a partial agonist action, abolished the orexin-induced secretory response but did not affect secretion induced by the muscarinic agonist bethanechol. Atropine, in contrast, inhibited bethanechol but not orexin-induced secretion. Orexin-A infused into the brain ventricles (2-20 nmol.kg(-1).h(-1)) or added to luminal perfusate (1.0-100 nM) did not affect secretion, indicating that orexin-A acts peripherally and at basolateral receptors. Overnight fasting decreased mucosal OX1 and OX2 mRNA expression (P < 0.01) as well as OX1 protein expression (P < 0.05). We conclude that stimulation of secretion by orexin-A may involve both receptor types and is independent of cholinergic pathways. Intestinal OX receptors and secretory responses are markedly related to food intake.

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“…In addition to the local intestinal control, the alkaline secretion is under central nervous influence. Up to fourfold increases in secretion occur after intracerebroventricular infusion of the ␣ 1 -adrenoceptor agonist phenylephrine (20,34), and stimulation has also been observed after intracerebroventricular administration of some neuropeptides (13, 21) and benzodiazepines (29). Vagal and sympathetic nerves as well as ␤-endorphin released from the pituitary gland mediate the centrally elicited influence on duodenal HCO 3 Ϫ secretion.…”

mentioning

confidence: 99%

Melatonin-induced calcium signaling in clusters of human and rat duodenal enterocytes

Sjöblom

Säfsten

Flemström

2003

American Journal of Physiology-Gastrointestinal and Liver Physi

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Sjö blom, Markus, Bengt Sä fsten, and Gunnar Flemströ m. Melatonin-induced calcium signaling in clusters of human and rat duodenal enterocytes. Am J Physiol Gastrointest Liver Physiol 284: G1034-G1044, 2003. First published February 12, 2003 10.1152/ajpgi.00500.2002The amount of melatonin present in enterochromaffin cells in the alimentary tract is much higher than that in the central nervous system, and melatonin acting at MT2 receptors mediates neural stimulation of mucosal HCO 3 Ϫ secretion in duodenum in vivo. We have examined effects of melatonin and receptor ligands on intracellular free calcium concentration ([Ca 2ϩ ]i) signaling in human and rat duodenal enterocytes. Clusters of interconnecting enterocytes (10-50 cells) were isolated by mild digestion (collagenase/dispase) of human duodenal biopsies or rat duodenal mucosa loaded with fura-2 AM and attached to the bottom of a temperature-controlled perfusion chamber. Clusters provided viable preparations and respond to stimuli as a syncytium. Melatonin and melatonin receptor agonists 2-iodo-N-butanoyl-5-methoxytryptamine and 2-iodomelatonin (1.0-100 nM) increased enterocyte [Ca 2ϩ ]i, EC50 of melatonin being 17.0 Ϯ 2.6 nM. The MT2 receptor antagonists luzindole and N-pentanoyl-2-benzyltryptamine abolished the [Ca 2ϩ ]i responses. The muscarinic antagonist atropine (1.0 M) was without effect on basal [Ca 2ϩ ]i and did not affect the response to melatonin. In the main type of response, [Ca 2ϩ ]i spiked rapidly and returned to basal values within 4-6 min. In another type, the initial rise in [Ca 2ϩ ]i was followed by rhythmic oscillations of high amplitude. Melatonin-induced enterocyte [Ca 2ϩ ]i signaling as well as mucosal cell-to-cell communication may be involved in stimulation of duodenal mucosal HCO 3 Ϫ secretion. enterochromaffin cells; enterocyte clusters; intracellular calcium; mucosal protection; syncytium DUODENAL MUCOSAL HCO 3 Ϫ SECRETION has a key role in duodenal protection against the pulses of hydrochloric acid (and pepsin) intermittently discharged from the stomach. The duodenal enterocytes transport HCO 3 Ϫ into the continuous layer of viscoelastic mucus gel on top of the epithelial surface, maintaining pH in its cell-facing portion at neutrality despite high acidities (pH Յ 2.0) in the duodenal luminal bulk solution. The major physiological stimulant of the HCO 3 Ϫ secretion is gastric acid expelled into the duodenal lumen, and the acid-induced HCO 3 Ϫ response is mediated by enteric nervous pathways, involving release of vasoactive intestinal polypeptide and acetylcholine (11, 12), as well as by E-type prostaglandins released from mucosal cells (36). In addition to the local intestinal control, the alkaline secretion is under central nervous influence. Up to fourfold increases in secretion occur after intracerebroventricular infusion of the ␣ 1 -adrenoceptor agonist phenylephrine (20,34), and stimulation has also been observed after intracerebroventricular administration of some neuropeptides (13, 21) and benzodiazepines (29)....

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Intracerebral adrenoceptor agonists influence rat duodenal mucosal bicarbonate secretion

Cited by 13 publications

References 0 publications

Peripheral melatonin mediates neural stimulation of duodenal mucosal bicarbonate secretion

Peripheral melatonin mediates neural stimulation of duodenal mucosal bicarbonate secretion

Food-induced expression of orexin receptors in rat duodenal mucosa regulates the bicarbonate secretory response to orexin-A

Melatonin-induced calcium signaling in clusters of human and rat duodenal enterocytes

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