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Article: Role of cholecystokinin in the intestinal fat- and acid-induced inhibition of gastric secretion.

Konturek, S J / Bilski, J / Cieszkowski, M

1992 Volume 42, Issue 1-2, Page(s) 97–109

Abstract: This study was designed to determine the role of cholecystokinin (CCK) in the inhibition of gastric HCl secretion by duodenal peptone, fat and acid in dogs with chronic gastric and pancreatic fistulas. Intraduodenal instillation of 5% peptone stimulated ... ...

Abstract	This study was designed to determine the role of cholecystokinin (CCK) in the inhibition of gastric HCl secretion by duodenal peptone, fat and acid in dogs with chronic gastric and pancreatic fistulas. Intraduodenal instillation of 5% peptone stimulated both gastric HCl secretion and pancreatic protein secretion and caused significant increments in plasma gastrin and CCK levels. L-364,718, a selective antagonist of CCK-A receptors, caused further increase in gastric HCl and plasma gastrin responses to duodenal peptone but reduced the pancreatic protein outputs in these tests by about 75%. L-365,260, an antagonist of type B receptors, reduced gastric acid by about 25% but failed to influence pancreatic response to duodenal peptone. Addition of 10% oleate or acidification of peptone to pH 3.0 profoundly inhibited acid secretion while significantly increasing the pancreatic protein secretion and plasma CCK levels. Administration of L-364,718 reversed the fall in gastric HCl secretion and significantly attenuated pancreatic protein secretion in tests with both peptone plus oleate and peptone plus acid. Exogenous CCK infused i.v. in a dose (25 pmol/kg per h) that raised plasma CCK to the level similar to that achieved by peptone meal plus fat resulted in similar inhibition of gastric acid response to that attained with fat and this effect was completely abolished by the pretreatment with L-364,718. We conclude that CCK released by intestinal peptone meal, containing fat or acid, exerts a tonic inhibitory influence on gastric acid secretion and gastrin release through the CCK-A receptors.
MeSH term(s)	Animals ; Benzodiazepinones/pharmacology ; Bethanechol Compounds/pharmacology ; Cholecystokinin/antagonists & inhibitors ; Cholecystokinin/blood ; Cholecystokinin/physiology ; Devazepide ; Dogs ; Gastric Acid/metabolism ; Gastric Fistula ; Gastrins/blood ; Histamine/pharmacology ; Hydrogen-Ion Concentration ; Oleic Acid ; Oleic Acids/pharmacology ; Pancreatic Fistula ; Peptones/pharmacology ; Phenylurea Compounds ; Receptors, Cholecystokinin/antagonists & inhibitors ; Sincalide/pharmacology
Chemical Substances	Benzodiazepinones ; Bethanechol Compounds ; Gastrins ; Oleic Acids ; Peptones ; Phenylurea Compounds ; Receptors, Cholecystokinin ; Oleic Acid (2UMI9U37CP) ; L 365260 (370JHF4586) ; Histamine (820484N8I3) ; Cholecystokinin (9011-97-6) ; Devazepide (JE6P7QY7NH) ; Sincalide (M03GIQ7Z6P)
Language	English
Publishing date	1992-11-20
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	225685-x
ISSN	1873-1686 ; 0167-0115
ISSN (online)	1873-1686
ISSN	0167-0115
DOI	10.1016/0167-0115(92)90027-r
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Article: Role of cholecystokinin in the inhibition of gastric acid secretion in dogs.

Konturek, S J / Bilski, J / Tasler, J / Cieszkowski, M

The Journal of physiology

1992 Volume 451, Page(s) 477–489

Abstract: 1. This study was designed to determine the involvement of cholecystokinin (CCK) in the gastric secretory responses to exogenous and endogenous secretagogues in conscious dogs with chronic gastric fistulae (GF), pancreatic fistulae (PF) and Heidenhain ... ...

Abstract	1. This study was designed to determine the involvement of cholecystokinin (CCK) in the gastric secretory responses to exogenous and endogenous secretagogues in conscious dogs with chronic gastric fistulae (GF), pancreatic fistulae (PF) and Heidenhain pouches (HP). 2. A meal of meat or intragastric application of peptone (300 mosM) increased secretion of HCl from the HP and pancreatic secretion of protein and plasma levels of gastrin, CCK and somatostatin. 3. The CCK receptor antagonist L-364,718 caused a further increase in the postprandial HCl secretion from the HP and in the plasma levels of gastrin and CCK but pancreatic output of protein and plasma concentration of somatostatin were significantly reduced. 4. Addition to intragastric peptone of 10% oleate or its acidification to pH 3.0 profoundly inhibited the HP secretion and gastrin release but significantly increased pancreatic secretion of protein and plasma levels of CCK and somatostatin. Administration of L-364,718 reversed the fall in the HP secretion and plasma gastrin while significantly attenuating pancreatic protein secretion and plasma somatostatin levels. 5. Intragastric administration of hyperosmolar (1200 mosM) peptone also inhibited HCl secretion from the HP but this was not affected by L-364,718. 6. Exogenous CCK and bombesin (but not gastrin) caused a small increase in HCl secretion from the HP and marked stimulation of pancreatic protein secretion accompanied by a significant rise in plasma levels of gastrin, CCK and somatostatin. Administration of L-364,718 resulted in a further increase in the HCl response of HP to bombesin and in plasma levels of gastrin and CCK but caused a reduction in plasma levels of somatostatin. 7. We conclude that CCK released by a meal of meat, intragastric peptone, oleate or acidified peptone and intravenous bombesin exerts tonic inhibitory influences on gastric acid secretion and that this effect is mediated, at least in part, by somatostatin.
MeSH term(s)	Animals ; Benzodiazepinones/pharmacology ; Cholecystokinin/antagonists & inhibitors ; Cholecystokinin/physiology ; Devazepide ; Dogs ; Eating/physiology ; Gastric Acid/metabolism ; Gastric Mucosa/drug effects ; Gastric Mucosa/metabolism ; Gastrins/metabolism ; Peptones/administration & dosage ; Receptors, Cholecystokinin/drug effects ; Receptors, Cholecystokinin/physiology
Chemical Substances	Benzodiazepinones ; Gastrins ; Peptones ; Receptors, Cholecystokinin ; Cholecystokinin (9011-97-6) ; Devazepide (JE6P7QY7NH)
Language	English
Publishing date	1992
Publishing country	England
Document type	Journal Article
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/jphysiol.1992.sp019174
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Article: The effects of ammonia on pancreatic enzyme secretion in vivo and in vitro.

Jaworek, J / Bilski, J / Jachimczak, B / Cieszkowski, M / Kot, M / Bielański, W / Konturek, S J

Journal of physiology and pharmacology : an official journal of the Polish Physiological Society

2000 Volume 51, Issue 2, Page(s) 315–332

Abstract: Background: Recent studies clearly demonstrate that Helicobacter pylori (H. pylori) infection of the stomach causes persistent elevation of ammonia (NH3) in gastric juice leading to hypergastrinemia and enhanced pancreatic enzyme secretion.: Methods: ...

Abstract	Background: Recent studies clearly demonstrate that Helicobacter pylori (H. pylori) infection of the stomach causes persistent elevation of ammonia (NH3) in gastric juice leading to hypergastrinemia and enhanced pancreatic enzyme secretion. Methods: The aim of this study is to evaluate the influence of NH4OH on plasma gastrin level and exocrine pancreatic secretion in vivo in conscious dogs equipped with chronic pancreatic fistulas and on secretory activity of in vitro isolated acini obtained from the rat pancreas by collagenase digestion. The effects of NH4OH on amylase release from pancreatic acini were compared with those produced by simple alkalization of these acini with NaOH. Results: NH4OH given intraduodenally (i.d.) in increasing concentrations (0.5, 1.0, 2.0, 4.0, or 8.0 mM/L) resulted in an increase of pancreatic protein output, reaching respectively 9%, 10%, 19%, 16% and 17% of caerulein maximum in these animals and in a marked increase in plasma gastrin level. NH4OH (8 x 0 mM/L, i.d.) given during intravenous (i.v.) infusion of secretin (50 pmol/kg-h) and cholecystokinin (50 pmol/kg-h) reduced the HCO3 and protein outputs by 35% and 37% respectively, as compared to control obtained with infusion of secretin plus cholecystokinin alone. When pancreatic secretion was stimulated by ordinary feeding the same amount of NH4OH administered i.d. decreased the HCO3- and protein responses by 78% and 47% respectively, and had no significant effect on postprandial plasma gastrin. In isolated pancreatic acini, increasing concentrations of NH4OH (10(-7)-10(-4) M) produced a concentration-dependent stimulation of amylase release, reaching about 43% of caerulein-induced maximum. When various concentrations of NH4OH were added to submaximal concentration of caerulein (10(-12) M) or urecholine (10(-5) M), the enzyme secretion was reduced at a dose 10(-5) M of NH4OH by 38% or 40%, respectively. Simple alkalization with NaOH of the incubation medium up to pH 8.5 markedly stimulated basal amylase secretion from isolated pancreatic acini, whereas the secretory response of these acini to pancreatic secretagogues was significantly diminished by about 30%. LDH release into the incubation medium was not significantly changed in all tests indicating that NH4OH did not produce any apparent damage of pancreatic acini and this was confirmed by histological examination of these acini. Conclusions: 1. NH4OH affects basal and stimulated pancreatic secretion. 2. The excessive release of gastrin may be responsible for the stimulation of basal pancreatic enzyme secretion in conscious animals, and 3. The inhibitory effects of NH4OH on stimulated secretion might be mediated, at least in part, by its direct action on the isolated pancreatic acini possibly due to the alkalization of these acini.
MeSH term(s)	Alkalies/pharmacology ; Ammonia/pharmacology ; Ammonium Hydroxide ; Amylases/metabolism ; Animals ; Bethanechol Compounds/pharmacology ; Ceruletide/pharmacology ; Dogs ; Eating/physiology ; Enzymes/drug effects ; Enzymes/metabolism ; Gastrins/blood ; Hydroxides/pharmacology ; In Vitro Techniques ; L-Lactate Dehydrogenase/metabolism ; Pancreas/enzymology ; Pancreas/secretion ; Sodium Hydroxide/pharmacology
Chemical Substances	Alkalies ; Bethanechol Compounds ; Enzymes ; Gastrins ; Hydroxides ; Ammonium Hydroxide (5138Q19F1X) ; Sodium Hydroxide (55X04QC32I) ; Ammonia (7664-41-7) ; Ceruletide (888Y08971B) ; L-Lactate Dehydrogenase (EC 1.1.1.27) ; Amylases (EC 3.2.1.-)
Language	English
Publishing date	2000-06
Publishing country	Poland
Document type	Journal Article
ZDB-ID	1125221-2
ISSN	1899-1505 ; 0867-5910 ; 0044-6033
ISSN (online)	1899-1505
ISSN	0867-5910 ; 0044-6033
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Article: Role of endogenous nitric oxide in the control of gastric acid secretion, blood flow and gastrin release in conscious dogs.

Bilski, J / Konturek, P C / Konturek, S J / Cieszkowski, M / Czarnobilski, K

Regulatory peptides

1994 Volume 53, Issue 3, Page(s) 175–184

Abstract: Nitric oxide (NO) was shown to mediate gastric hyperemia following secretory stimulation but its role in the control of gastric secretion has not been clarified. Secretory studies were carried out on conscious dogs with chronic gastric fistula, ... ...

Abstract	Nitric oxide (NO) was shown to mediate gastric hyperemia following secretory stimulation but its role in the control of gastric secretion has not been clarified. Secretory studies were carried out on conscious dogs with chronic gastric fistula, Heidenhain pouch and esophageal fistula, while changes in gastric blood flow were measured in the mucosa of Heidenhain pouuch by laser Doppler flowmetry. Plasma gastrin was determined by radioimmunoassay. Infusion of NG-nitro-L-arginine (L-NNA) (bolus i.v. injection of 2.5 mg/kg followed by infusion of 0.5 mg/kg/h), a potent inhibitor of nitric oxide synthase, failed to affect basal gastric secretion or plasma gastrin level but suppressed an increase of this secretion induced by sham-feeding, ordinary meat feeding or i.v. infusion of bombesin (0.5 microgram/kg/h), pentagastrin (4 micrograms/kg/h) or histamine (40 micrograms/kg/h). In tests with feeding and bombesin infusion, L-NNA caused a significant and dose-dependent reduction in plasma gastrin levels. The inhibition by L-NNA of gastric acid secretory response to pentagastrin, histamine or feeding was accompanied by a decline in blood flow. Addition of L-arginine (bolus i.v. dose of 50 mg/kg followed by infusion of 5 mg/kg/h) significantly attenuated the L-NNA induced inhibition of gastric secretion and the reduction in plasma gastrin response as well as in the fall of gastric blood flow. We conclude that endogenous nitric oxide affects the gastric secretion and that this effect is mediated, at least in part, by the changes in the gastrin release and gastric blood flow.
MeSH term(s)	Animals ; Arginine/analogs & derivatives ; Arginine/pharmacology ; Bombesin/administration & dosage ; Bombesin/pharmacology ; Dogs ; Eating ; Fistula ; Gastric Acid/metabolism ; Gastric Mucosa/drug effects ; Gastrins/metabolism ; Histamine/administration & dosage ; Histamine/pharmacology ; Infusions, Intravenous ; Muscle, Smooth/blood supply ; Nitric Oxide/physiology ; Nitroarginine ; Pentagastrin/administration & dosage ; Pentagastrin/pharmacology ; Regional Blood Flow/drug effects ; Stomach/blood supply ; Time Factors
Chemical Substances	Gastrins ; Nitroarginine (2149-70-4) ; Nitric Oxide (31C4KY9ESH) ; Histamine (820484N8I3) ; Arginine (94ZLA3W45F) ; Pentagastrin (EF0NX91490) ; Bombesin (PX9AZU7QPK)
Language	English
Publishing date	1994-10-21
Publishing country	Netherlands
Document type	Comparative Study ; Journal Article
ZDB-ID	225685-x
ISSN	1873-1686 ; 0167-0115
ISSN (online)	1873-1686
ISSN	0167-0115
DOI	10.1016/0167-0115(94)90166-x
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Article: Role of endogenous nitric oxide in the control of canine pancreatic secretion and blood flow.

Konturek, S J / Bilski, J / Konturek, P K / Cieszkowski, M / Pawlik, W

Gastroenterology

1993 Volume 104, Issue 3, Page(s) 896–902

Abstract: Background: Endogenous nitric oxide has been implicated in the control of mesenteric circulation, but its role in the control of pancreatic blood flow and exocrine pancreatic secretion has not been studied.: Methods: Secretory studies were performed ... ...

Abstract	Background: Endogenous nitric oxide has been implicated in the control of mesenteric circulation, but its role in the control of pancreatic blood flow and exocrine pancreatic secretion has not been studied. Methods: Secretory studies were performed on conscious dogs with chronic pancreatic fistulas, and changes in pancreatic blood flow were measured by laser Doppler flowmetry in anesthetized animals. Results: Infusion of NG-nitro-L-arginine did not affect basal pancreatic protein secretion but suppressed an increase of this secretion induced by L-arginine but not that induced by glyceryl trinitrate. Sham-feeding, meal feeding, and infusion of secretin plus cholecystokinin induced pancreatic protein outputs reaching, respectively, 30%, 74%, and 50% of cerulein maximum in these dogs. Infusion of NG-nitro-L-arginine caused a profound inhibition of these secretions, whereas the addition of L-arginine reversed this inhibition in part. NG-nitro-L-arginine or L-arginine added to the incubation medium of isolated canine pancreatic acini did not affect basal or cholecystokinin-induced amylase release. In anesthetized dogs, infusion of NG-nitro-L-arginine caused a significant reduction in the pancreatic blood flow both while resting and following stimulation with secretin plus cholecystokinin but did not affect this flow in animals treated with glyceryl trinitrate. Addition of L-arginine attenuated the decrease in pancreatic blood flow and the increase in systemic blood pressure caused by NG-L-nitro-arginine. Conclusions: Endogenous NO affects pancreatic secretion probably through the changes in the vascular bed.
MeSH term(s)	Amylases/metabolism ; Animals ; Arginine/analogs & derivatives ; Arginine/pharmacology ; Dogs ; In Vitro Techniques ; Nitric Oxide/metabolism ; Nitroarginine ; Nitroglycerin/pharmacology ; Pancreas/blood supply ; Pancreas/drug effects ; Pancreas/metabolism ; Regional Blood Flow/drug effects
Chemical Substances	Nitroarginine (2149-70-4) ; Nitric Oxide (31C4KY9ESH) ; Arginine (94ZLA3W45F) ; Amylases (EC 3.2.1.-) ; Nitroglycerin (G59M7S0WS3)
Language	English
Publishing date	1993-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	80112-4
ISSN	1528-0012 ; 0016-5085
ISSN (online)	1528-0012
ISSN	0016-5085
DOI	10.1016/0016-5085(93)91028-g
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Article: Antagonism of receptors for gastrin, cholecystokinin and GRP/bombesin in postprandial stimulation of exocrine pancreas in dogs.

Konturek, S J / Tasler, J / Bilski, J / Cieszkowski, M / Cai, R Z / Schally, A V

Journal of physiology and pharmacology : an official journal of the Polish Physiological Society

1993 Volume 44, Issue 1, Page(s) 43–53

Abstract: Postprandial pancreatic secretion results from the interaction of neural and hormonal factors such as cholecystokinin (CCK), gastrin and gastrin releasing peptide (GRP), but their contribution to the net secretion is not established. Recent description ... ...

Abstract	Postprandial pancreatic secretion results from the interaction of neural and hormonal factors such as cholecystokinin (CCK), gastrin and gastrin releasing peptide (GRP), but their contribution to the net secretion is not established. Recent description of highly specific and potent hormonal receptor antagonists allows the determination of the physiological role of CCK, gastrin and GRP. In six dogs with chronic pancreatic fistulas, the blockade of CCK receptors by L-364, 718, gastrin receptors by L-365, 260 or GRP/bombesin receptors by nonapeptide RC-3095 failed to affect basal or sham-feeding induced pancreatic secretion indicating that none of these hormonal peptides plays a major role in this secretion. In contrast, the pancreatic response to ordinary feeding (which includes cephalic, gastric and intestinal phases), that was accompanied by a significant increment in plasma CCK and gastrin levels, was strongly inhibited (by over 50%) by L-364, 718 and slightly (by 20-30%) by L-365, 260 but not by RC-3095. Each antagonist was given at a dose that eliminated the secretory response to CCK, gastrin or GRP, respectively. We conclude that specific receptor antagonists are useful tools in assessing the physiological role of gut hormones in the control of pancreatic secretion and that none of the peptides tested appears to be involved in the cephalic phase. However, CCK plays a major role in the postprandial stimulation of pancreatic secretion.
MeSH term(s)	Animal Feed ; Animals ; Benzodiazepinones/pharmacology ; Bombesin/analogs & derivatives ; Bombesin/antagonists & inhibitors ; Bombesin/pharmacology ; Cholecystokinin/antagonists & inhibitors ; Devazepide ; Dogs ; Eating/physiology ; Meat ; Pancreas/drug effects ; Pancreas/metabolism ; Peptide Fragments/pharmacology ; Phenylurea Compounds ; Protein Biosynthesis ; Receptors, Bombesin ; Receptors, Cholecystokinin/antagonists & inhibitors ; Receptors, Neurotransmitter/antagonists & inhibitors
Chemical Substances	Benzodiazepinones ; Peptide Fragments ; Phenylurea Compounds ; Receptors, Bombesin ; Receptors, Cholecystokinin ; Receptors, Neurotransmitter ; bombesin (6-14), Tpi(6)-Leu(13)-psi(CH2NH)-Leu(14)- (138147-78-1) ; L 365260 (370JHF4586) ; Cholecystokinin (9011-97-6) ; Devazepide (JE6P7QY7NH) ; Bombesin (PX9AZU7QPK)
Language	English
Publishing date	1993-03
Publishing country	Poland
Document type	Journal Article
ZDB-ID	1125221-2
ISSN	1899-1505 ; 0867-5910 ; 0044-6033
ISSN (online)	1899-1505
ISSN	0867-5910 ; 0044-6033
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Article: Role of liver and intestines in the degradation of epidermal growth factor.

Konturek, S J / Tasler, J / Bielanski, W / Cieszkowski, M / Pawlik, W

Digestion

1990 Volume 45, Issue 4, Page(s) 202–211

Abstract: Epidermal growth factor (EGF) is widely distributed in the gastrointestinal tissues and released into the gut lumen but its physiological role is questionable because of the postulated high uptake and degradation of this peptide in the liver. This study ... ...

Abstract	Epidermal growth factor (EGF) is widely distributed in the gastrointestinal tissues and released into the gut lumen but its physiological role is questionable because of the postulated high uptake and degradation of this peptide in the liver. This study was designed to examine the action of EGF administered intraduodenally (i.d.), intravenously (i.v.) or intraportally (i.p.) on pentagastrin-stimulated gastric and pancreatic secretion and to determine the role of liver in the EGF uptake. In conscious dogs with gastric and pancreatic fistulas, EGF infused i.v. or i.p. in graded doses (0.12-1.0 microgram/kg.h) caused a dose-dependent inhibition of pentagastrin-induced gastric H+ secretion without alteration in pancreatic protein secretion. EGF infused i.v. and i.p. raised significantly plasma levels of the peptide but these increments were significantly lower with i.p. than with i.v. infusion. EGF given i.d. did not affect gastric or pancreatic secretion and failed to raise significantly plasma EGF level. In anesthetized dogs, no difference was found in the basal plasma EGF levels between arterial and portal or hepatic blood. during i.v. infusion of EGF, plasma EGF level in hepatic venous blood was about 40% lower and that in the portal blood was about 30% lower than that in arterial blood indicating a marked uptake of peptide during the passage through the liver and the intestines, respectively. EGF was present in negligible amounts in gastric secretion but appeared in nanogram concentrations in the pancreatic secretion and increased after pentagastrin stimulation. We conclude that (1) the liver and the intestines are almost equally involved in partial degradation of EGF and that the kidneys may also contribute to the elimination of circulating EGF; (2) the uptake of EGF by these organs is limited and can be overcome by increasing doses of infused EGF, and (3) absorption of EGF from the intestinal lumen does not contribute to its circulating concentrations.
MeSH term(s)	Animals ; Dogs ; Epidermal Growth Factor/metabolism ; Epidermal Growth Factor/pharmacokinetics ; Epidermal Growth Factor/physiology ; Gastric Acid/secretion ; Humans ; Intestines/metabolism ; Kidney/metabolism ; Liver/metabolism ; Pancreatic Juice/secretion ; Pentagastrin/pharmacology ; Stimulation, Chemical
Chemical Substances	Epidermal Growth Factor (62229-50-9) ; Pentagastrin (EF0NX91490)
Language	English
Publishing date	1990
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1712-7
ISSN	1421-9867 ; 0012-2823
ISSN (online)	1421-9867
ISSN	0012-2823
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Article: Comparison of telenzepine, pirenzepine and atropine on gastric acid and pepsin secretion in response to histamine, pentagastrin, bethanechol, sham-feeding and feeding.

Konturek, S J / Tasler, J / Cieszkowski, M / Szewczyk, K / Kromer, W

Digestion

1989 Volume 44, Issue 2, Page(s) 66–78

Abstract: This study was designed to compare gastric antisecretory effects of telenzepine, a new antimuscarinic agent, with those of pirenzepine and atropine in dogs. None of these antimuscarinics affected gastric acid secretion induced by histamine but all of ... ...

Abstract	This study was designed to compare gastric antisecretory effects of telenzepine, a new antimuscarinic agent, with those of pirenzepine and atropine in dogs. None of these antimuscarinics affected gastric acid secretion induced by histamine but all of them caused a dose-dependent inhibition of acid secretion from the gastric fistula (GF) and Heidenhain pouches (HP) stimulated by pentagastrin and bethanechol, telenzepine being 5-9 times more potent than pirenzepine and equipotent with atropine. All antimuscarinics were also effective inhibitors of acid responses to sham feeding and ordinary feeding. The inhibitory effect of telenzepine and pirenzepine were not accompanied by any major alterations in plasma gastrin or somatostatin but those of atropine were related to significant increase in plasma gastrin and to significant decrease in plasma somatostatin levels, suggesting the involvement of M2 receptors in the cholinergic control of these hormones. All three antimuscarinics were effective inhibitors of pepsin secretion induced both from the GF and HP by all secretagogues used. Neither telenzepine nor pirenzepine administered in various doses affected the heart rate while atropine caused a significant increase in heart rate confirming that the former agents are selective M1 receptor antagonists. This study provides evidence that telenzepine is more potent than pirenzepine in the inhibition of gastric secretion induced by pentagastrin, bethanechol, sham-feeding and ordinary feeding and that, unlike atropine, it does not increase plasma gastrin responses to meat feeding. In fact, telenzepine and pirenzepine alike reduced plasma gastrin concentrations under these conditions. No influence of these antimuscarinics on plasma somatostatin levels was observed.
MeSH term(s)	Animals ; Atropine/pharmacology ; Bethanechol ; Bethanechol Compounds/pharmacology ; Dogs ; Food ; Gastric Acid/secretion ; Gastric Fistula/physiopathology ; Histamine/pharmacology ; Parasympatholytics/pharmacology ; Pentagastrin/pharmacology ; Pepsin A/secretion ; Pirenzepine/analogs & derivatives ; Pirenzepine/pharmacology ; Stomach/physiology
Chemical Substances	Bethanechol Compounds ; Parasympatholytics ; Bethanechol (004F72P8F4) ; telenzepine (0990EG3K10) ; Pirenzepine (3G0285N20N) ; Atropine (7C0697DR9I) ; Histamine (820484N8I3) ; Pepsin A (EC 3.4.23.1) ; Pentagastrin (EF0NX91490)
Language	English
Publishing date	1989
Publishing country	Switzerland
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1712-7
ISSN	1421-9867 ; 0012-2823
ISSN (online)	1421-9867
ISSN	0012-2823
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Article: Effect of cholecystokinin receptor antagonist on pancreatic responses to exogenous gastrin and cholecystokinin and to meal stimuli.

Konturek, S J / Tasler, J / Cieszkowski, M / Szewczyk, K / Hladij, M

Gastroenterology

1988 Volume 94, Issue 4, Page(s) 1014–1023

Abstract: Exocrine pancreatic response to food is believed to result from the interaction of neural and hormonal factors, but their contribution in the net postprandial secretion is unknown. Recent description of a highly specific and potent cholecystokinin (CCK)- ... ...

Abstract	Exocrine pancreatic response to food is believed to result from the interaction of neural and hormonal factors, but their contribution in the net postprandial secretion is unknown. Recent description of a highly specific and potent cholecystokinin (CCK)-receptor antagonist permitted the evaluation of the physiologic role of CCK in postprandial pancreatic secretion. In dogs with chronic pancreatic fistula, CCK antagonism caused little alteration in sham feeding- or urecholine-induced pancreatic protein secretion, but reduced by approximately 60% the pancreatic protein response to a gastrointestinal meal and virtually abolished the pancreatic responses to duodenal perfusion with amino acids or oleate and to exogenous CCK, but not to secretin or neurotensin. The pancreatic protein responses, particularly to lower doses of gastrin, were also reduced by CCK-receptor antagonist, but no changes in the responses to secretin or neurotensin were detected. Cholecystokinin antagonism also significantly reduced the pancreatic polypeptide responses to CCK, gastrin, and the gastrointestinal meal, possibly due to removal of the CCK-mediated release of pancreatic polypeptide. We conclude that CCK plays a crucial role in the mediation of the gastrointestinal phase, but not the cephalic phase, of pancreatic secretion.
MeSH term(s)	Animals ; Cholecystokinin/physiology ; Dogs ; Food ; Gastric Fistula/physiopathology ; Gastrins/pharmacology ; Gastrins/physiology ; Glutamine/analogs & derivatives ; Pancreas/metabolism ; Pancreatic Fistula/physiopathology ; Pancreatic Polypeptide/metabolism ; Proglumide/analogs & derivatives ; Proglumide/pharmacology ; Receptors, Cholecystokinin/drug effects
Chemical Substances	Gastrins ; Receptors, Cholecystokinin ; Glutamine (0RH81L854J) ; Pancreatic Polypeptide (59763-91-6) ; Cholecystokinin (9011-97-6) ; Proglumide (EPL8W5565D) ; lorglumide (LAD1UQ73BE)
Language	English
Publishing date	1988-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80112-4
ISSN	1528-0012 ; 0016-5085
ISSN (online)	1528-0012
ISSN	0016-5085
DOI	10.1016/0016-5085(88)90561-6
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Article: Gastric acid response to topical or intravenous histamine and topical H2-receptor blockade in dogs.

Konturek, S J / Cieszkowski, M / Kwiecień, N / Harrison, C

Agents and actions

1981 Volume 11, Issue 5, Page(s) 437–441

Abstract: This study was undertaken to determine gastric acid surface and to examine the local effect f ranitidine, a histamine H2-receptor antagonist, on the gastric acid response to histamine. Histamine applied to the Heidenhain pouch (HP) mucosa resulted in a ... ...

Abstract	This study was undertaken to determine gastric acid surface and to examine the local effect f ranitidine, a histamine H2-receptor antagonist, on the gastric acid response to histamine. Histamine applied to the Heidenhain pouch (HP) mucosa resulted in a slight and dose-dependent stimulation of acid secretion without affecting acid secretion from the main stomach. Ranitidine given into the HP caused dose-dependent inhibition of the HP response to topical or intravenous histamine without affecting the acid response of the main stomach and without any significant change in the serum ranitidine level. Ranitidine applied to the main stomach with the pylorus occluded inhibited histamine-induced acid secretion also without any increase in the serum ranitidine level. This inhibition was about 30% of that obtained with the same dose of ranitidine given into the stomach with the pylorus left open during the experiment. This study provides evidence that topical histamine is a weak stimulant of gastric secretion and that topical ranitidine is capable of local inhibition of the acid response to both topical and intravenous histamine.
MeSH term(s)	Administration, Topical ; Animals ; Dogs ; Furans/pharmacology ; Gastric Acid/metabolism ; Gastric Mucosa/drug effects ; Histamine/administration & dosage ; Histamine/pharmacology ; Histamine H2 Antagonists/pharmacology ; Infusions, Parenteral ; Ranitidine
Chemical Substances	Furans ; Histamine H2 Antagonists ; Histamine (820484N8I3) ; Ranitidine (884KT10YB7)
Language	English
Publishing date	1981-11
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	80022-3
ISSN	0065-4299
ISSN	0065-4299
DOI	10.1007/bf02004703
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