The Experts below are selected from a list of 99 Experts worldwide ranked by ideXlab platform
Gunnar Flemström - One of the best experts on this subject based on the ideXlab platform.
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Cholecystokinin but not ghrelin stimulates mucosal bicarbonate Secretion in rat duodenum: Independence of feeding status and cholinergic stimuli
Regulatory Peptides, 2013Co-Authors: Markus Sjöblom, Ramin Lindqvist, Magnus W. Bengtsson, Gunilla Jedstedt, Gunnar FlemströmAbstract:Abstract Cholecystokinin (CCK) is an important regulator of food digestion but its influence on small intestinal Secretion has received little attention. We characterized effects of CCK-8, ghrelin and some related peptides on Duodenal HCO 3 − Secretion in vivo and demonstrated CCK-induced calcium signaling in acutely isolated enterocytes. A segment of proximal duodenum with intact blood supply was cannulated in situ in anaesthetized rats. Mucosal HCO 3 − Secretion was continuously recorded (pH-stat). Peptides were administrated to the duodenum by close intra-arterial infusion. Clusters of Duodenal enterocytes were attached to the bottom of a perfusion chamber. The intracellular calcium concentration ([Ca 2 + ] i ) was examined by dual-wavelength imaging. CCK-8 (3.0, 15 and 60 pmol/kg,h) caused dose-dependent increases (p 2 -selective antagonist luzindole inhibited the rise in Secretion. Atropine decreased sensitivity to CCK-8. The appetite-related peptide ghrelin was without effect on the Duodenal Secretion in fasted as well as fed animals. Superfusion with CCK-8 (1.0-50 nM) induced [Ca 2 + ] i signaling in acutely isolated Duodenal enterocytes. After an initial peak response, [Ca 2 + ] i returned to near basal values within 3–5 min. Devazepide but not YMM022 inhibited this [Ca 2 + ] i response. Low doses of CCK-8 stimulate Duodenal alkaline Secretion and induce enterocyte [Ca 2 + ] i signaling by an action at CCK1 receptors. The results point to importance of CCK in the rapid postprandial rise in mucosa-protective Duodenal Secretion.
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Comprehensive Physiology - Secretion of Bicarbonate by Gastric and Duodenal Mucosa
Comprehensive Physiology, 2011Co-Authors: Gunnar Flemström, Andrew GarnerAbstract:The sections in this article are: 1 Methods of Measurement 1.1 Gastric Bicarbonate Secretion 1.2 Duodenal Bicarbonate Secretion 2 Mechanisms of GastroDuodenal Bicarbonate Secretion 2.1 Origin and Transport of Gastric Bicarbonate 2.2 Contribution of Bicarbonate Leakage 2.3 Duodenal Mucosal Transport of Bicarbonate 2.4 Gradient in Secretion Along the Duodenum 2.5 Biochemical Basis for Duodenal Bicarbonate Secretion 3 Physiological Control of GastroDuodenal Bicarbonate Secretion 3.1 Humoral Control 3.2 Neural Influence 3.3 Control by Mucosal Endogenous Prostaglandins 3.4 Relation to Gastric Acid Secretion and Blood Flow 4 Pharmacological Modulation 4.1 Inhibitors of Gastric Alkaline Secretion 4.2 Stimulation of Gastric Alkaline Secretion by Prostaglandins 4.3 Duodenal Mucosal Alkaline Secretion and cAMP 4.4 Stimulation of Duodenal Secretion by Prostaglandins 4.5 Other Drugs Affecting Duodenal Alkaline Secretion 5 Protective Role of Bicarbonate 5.1 Surface pH Gradient 5.2 Possible Therapeutic Implications 6 Summary and Perspectives
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Duodenal defence mechanisms: role of mucosal bicarbonate Secretion
InflammoPharmacology, 2002Co-Authors: Gunnar Flemström, Markus SjöblomAbstract:The Duodenal epithelium secretes bicarbonate at higher rates than does the stomach (or more distal small intestine) and the Duodenal Secretion is currently accepted as the most important defence mechanism against acid discharged from the stomach. HCO_3 ^- entering the continuous layer of visco-elastic mucus gel on top of the epithelial surface maintains pH in its cell-facing portion at neutrality at acidities encountered in the healthy duodenum. The Secretion is decreased in patients with acute and chronic Duodenal ulcer disease and is inhibited by non-steroidal anti-inflammatory agents. Studies of the neurohumoral control of the Duodenal alkaline Secretion and of acid/base transport processes and intracellular signaling in Duodenal enterocytes are currently of great research interest.
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Duodenal Protection: Influence of Melatonin and other Intestinal Transmitters on Duodenal Bicarbonate Secretion and Enterocyte Signaling
Mechanisms and Consequences of Proton Transport, 2002Co-Authors: Gunnar Flemström, Markus SjöblomAbstract:The Duodenal epithelium secretes HC03 - at higher rates than does the stomach (or more distal small intestine) and the Duodenal Secretion is currently accepted as the most important defence mechanism against acid discharged from the stomach (4,6). HC03 - entering the continuous layer of visco-elastic mucus gel on top of the epithelial surface maintains pH in its cell-facing portion at neutrality at acidities encountered in the healthy duodenum.
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Dopamine and the brain-gut axis.
Advances in pharmacology, 1997Co-Authors: Gunnar Flemström, Bengt Säfsten, L KnutsonAbstract:Publisher Summary Some dopaminergic compounds are reported to be efficient in the treatment of Duodenal ulcer disease in humans and prevent gastroDuodenal mucosal damage in animal models of ulcer disease. These findings in humans and animals made it of interest to investigate the effects of dopamine and dopaminergic compounds on Duodenal mucosal bicarbonate Secretion. The Secretion has been studied in anesthetized animals and in human volunteers. The results of these studies are summarized and some recent findings are reported in this chapter. Animal studies of effects of dopamine and dopaminergic compounds have to consider that well-documented sites of action are the central nervous system as well as some peripheral tissues, including the intestinal tract and the kidney. Dopamine may exert effects not only on dopamine receptors, but also on adrenoceptors. Dopamine D 1 -receptor stimulation by bromocriptine, in contrast, caused a decrease in Secretion. Catecholamine O-methyl transferase (COMT) inhibitors decrease tissue degradation of catecholamines, including dopamine. Interestingly, the centrally acting D 1 /D 2 antagonist haloperidol does not decrease but stimulates the Duodenal Secretion. Studies of isolated Duodenal enterocytes lend strong support to the suggestion that dopamine stimulates Duodenal mucosal bicarbonate Secretion by an action on the Duodenal enterocytes and confirm that stimulation is D 1 -receptor-mediated. On the other hand peripheral COMT inhibition increases Duodenal mucosal bicarbonate Secretion in human volunteers as well as in animals. These results indicate that Duodenal Secretion is stimulated via peripheral dopamine D 1 receptors. The stimulation of the Secretion by haloperidol may suggest the presence of central nervous as well as peripheral dopaminergic modulation of Duodenal bicarbonate Secretion and mucosal protection.
Wladyslaw Ochmanski - One of the best experts on this subject based on the ideXlab platform.
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neuroendocrinology of gastric h and Duodenal hco3 Secretion the role of brain gut axis
European Journal of Pharmacology, 2004Co-Authors: Peter C Konturek, S J Konturek, Wladyslaw OchmanskiAbstract:Gastric H+ and Duodenal HCO3− Secretions are precisely regulated by neuro-hormonal mechanisms at central and peripheral levels to match the rate of these Secretions with the type of stimulation of sensory receptors in the head area (sight, smell, taste, etc.) and in the gastro-intestinal system. Two-way communication pathways operate between the brain and the gut, each comprising afferent fibers signaling sensory information from the gut to the brain and efferent fibers transmitting signals in opposite direction. Short intramural and long extramural reflexes are triggered as well as various gut hormones are released by feeding that “cooperate” with the “brain–gut axis” in the alteration of exocrine and endocrine gastro-Duodenal Secretion, motility and blood circulation. The malfunction of gastric or Duodenal secretory mechanisms may lead to disturbances of gastric H+-pepsin or Duodenal mucus-HCO3− Secretion and to gastro-Duodenal disorders and diseases. This review presents recent advances in pathophysiological mechanisms underlying gastro-Duodenal secretory disorders.
Markus Sjöblom - One of the best experts on this subject based on the ideXlab platform.
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Cholecystokinin but not ghrelin stimulates mucosal bicarbonate Secretion in rat duodenum: Independence of feeding status and cholinergic stimuli
Regulatory Peptides, 2013Co-Authors: Markus Sjöblom, Ramin Lindqvist, Magnus W. Bengtsson, Gunilla Jedstedt, Gunnar FlemströmAbstract:Abstract Cholecystokinin (CCK) is an important regulator of food digestion but its influence on small intestinal Secretion has received little attention. We characterized effects of CCK-8, ghrelin and some related peptides on Duodenal HCO 3 − Secretion in vivo and demonstrated CCK-induced calcium signaling in acutely isolated enterocytes. A segment of proximal duodenum with intact blood supply was cannulated in situ in anaesthetized rats. Mucosal HCO 3 − Secretion was continuously recorded (pH-stat). Peptides were administrated to the duodenum by close intra-arterial infusion. Clusters of Duodenal enterocytes were attached to the bottom of a perfusion chamber. The intracellular calcium concentration ([Ca 2 + ] i ) was examined by dual-wavelength imaging. CCK-8 (3.0, 15 and 60 pmol/kg,h) caused dose-dependent increases (p 2 -selective antagonist luzindole inhibited the rise in Secretion. Atropine decreased sensitivity to CCK-8. The appetite-related peptide ghrelin was without effect on the Duodenal Secretion in fasted as well as fed animals. Superfusion with CCK-8 (1.0-50 nM) induced [Ca 2 + ] i signaling in acutely isolated Duodenal enterocytes. After an initial peak response, [Ca 2 + ] i returned to near basal values within 3–5 min. Devazepide but not YMM022 inhibited this [Ca 2 + ] i response. Low doses of CCK-8 stimulate Duodenal alkaline Secretion and induce enterocyte [Ca 2 + ] i signaling by an action at CCK1 receptors. The results point to importance of CCK in the rapid postprandial rise in mucosa-protective Duodenal Secretion.
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Duodenal defence mechanisms: role of mucosal bicarbonate Secretion
InflammoPharmacology, 2002Co-Authors: Gunnar Flemström, Markus SjöblomAbstract:The Duodenal epithelium secretes bicarbonate at higher rates than does the stomach (or more distal small intestine) and the Duodenal Secretion is currently accepted as the most important defence mechanism against acid discharged from the stomach. HCO_3 ^- entering the continuous layer of visco-elastic mucus gel on top of the epithelial surface maintains pH in its cell-facing portion at neutrality at acidities encountered in the healthy duodenum. The Secretion is decreased in patients with acute and chronic Duodenal ulcer disease and is inhibited by non-steroidal anti-inflammatory agents. Studies of the neurohumoral control of the Duodenal alkaline Secretion and of acid/base transport processes and intracellular signaling in Duodenal enterocytes are currently of great research interest.
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Duodenal Protection: Influence of Melatonin and other Intestinal Transmitters on Duodenal Bicarbonate Secretion and Enterocyte Signaling
Mechanisms and Consequences of Proton Transport, 2002Co-Authors: Gunnar Flemström, Markus SjöblomAbstract:The Duodenal epithelium secretes HC03 - at higher rates than does the stomach (or more distal small intestine) and the Duodenal Secretion is currently accepted as the most important defence mechanism against acid discharged from the stomach (4,6). HC03 - entering the continuous layer of visco-elastic mucus gel on top of the epithelial surface maintains pH in its cell-facing portion at neutrality at acidities encountered in the healthy duodenum.
Sandor Szabo - One of the best experts on this subject based on the ideXlab platform.
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Dopamine in gastrointestinal disease
Digestive Diseases and Sciences, 1990Co-Authors: Gary B. Glavin, Sandor SzaboAbstract:Dopamine is an important enteric neuromodulator. Herein we review the data that support a role for dopaminergic involvement in experimental Duodenal and gastric ulceration; gastric, pancreatic, and Duodenal Secretion; gastrointestinal motility; and gastric and intestinal submucosal blood flow regulation. There also is support for a role for dopamine and dopamimetic agents in the treatment of certain experimental gastrointestinal diseases because some highly selective dopamine agonists are gastroprotective when given either parenterally or centrally. Based upon these observations, we suggest that dopamine is a key element of the “brain-gut axis” and represents a potentially important target for pharmacotherapeutic exploitation.
O. B. Schaffalitzky De Muckadell - One of the best experts on this subject based on the ideXlab platform.
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Effects of oleic acid and endogenous bile on Duodenal Secretion of somatostatin in man
Digestive Diseases and Sciences, 1992Co-Authors: O. Olsen, J. J. Holst, O. B. Schaffalitzky De MuckadellAbstract:We studied the effects of intraDuodenal oleic acid on the release of somatostatin to plasma and the correlation between endogenous bile output and plasma somatostatin. In five normal persons infusion of 0, 5, 10, 20 and 40 mM oleic acid dose-dependently increased the levels of somatostatin during as well as after gallbladder emptying. The difference between somatostatin concentration during and after gallbladder emptying was not significant. The amylase Secretion also was significantly correlated to the dose of fat, whereas the output of bile salts was the same for all fat doses used. Our observations indicate that intraDuodenal oleic acid-and not bile salts-releases somatostatin from the gut.
