Gastrin is not a physiological regulator of pancreatic exocrine secretion in the dog

1987 ◽  
Vol 252 (1) ◽  
pp. G40-G44
Author(s):  
E. Kohler ◽  
C. Beglinger ◽  
V. Eysselein ◽  
U. Grotzinger ◽  
K. Gyr
Keyword(s):  
Pancreatic Secretion ◽  
Pancreatic Enzyme ◽  
Exocrine Secretion ◽  
Exocrine Pancreatic Secretion ◽  
Response Curves ◽  
Blood Concentrations ◽  
Pancreatic Enzyme Secretion ◽  
Pancreatic Exocrine ◽  
Bicarbonate Output

The role of gastrin as a regulator of exocrine pancreatic secretion has not been proven adequately. In the present study we therefore compared the relative molar potencies of sulfated and unsulfated gastrin 17 with structurally related CCK peptides (synthetic CCK-8 and natural porcine CCK-33) in stimulating exocrine pancreatic secretion in conscious dogs. Dose response curves were constructed for pancreatic and gastric acid secretion. Plasma gastrin levels after exogenous gastrin 17-I and -II were compared with postprandial gastrin concentrations (meal: ground beef 20 g/kg body wt). The molar potency estimates calculated with synthetic CCK8 as standard (potency = 1.00) for pancreatic protein secretion were natural porcine 50% pure CCK-33 1.60, gastrin 17-I 0.12, and gastrin 17-II 0.16. All four peptides induced a dose-dependent increase in pancreatic bicarbonate output. However, the blood concentrations needed to stimulate pancreatic secretion were above the postprandial gastrin levels. Our data indicate that both gastrin 17 peptides are not physiological regulators of pancreatic enzyme secretion in dogs.

Role of endogenous cholecystokinin on vagally stimulated pancreatic secretion in dogs

1989 ◽  
Vol 257 (6) ◽  
pp. G944-G949
Author(s):  
C. K. Kim ◽  
K. Y. Lee ◽  
T. Wang ◽  
G. Sun ◽  
T. M. Chang ◽  
...  
Keyword(s):  
Pancreatic Secretion ◽  
Plasma Concentrations ◽  
Exocrine Secretion ◽  
Vagus Nerves ◽  
Pancreatic Acini ◽  
Venous Circulation ◽  
Gut Hormone ◽  
Pancreatic Exocrine ◽  
Cck Receptor Antagonist

Pancreatic exocrine secretion was evoked by electrical stimulation of the vagus nerves (EVS) in dogs to determine whether a gut hormone was responsible for the pancreatic stimulatory activity. In 39 dogs, pancreatic juice was continuously collected to measure volume, bicarbonate, and amylase output, while portal and femoral venous plasma concentrations of gastrin, cholecystokinin (CCK), vasoactive intestinal polypeptide (VIP), and pancreatic polypeptide (PP) were determined by radioimmunoassay. EVS produced a significant increase in the pancreatic secretion. Although concentrations of all four peptides significantly increased in plasma, only CCK at the concentration in venous circulation was bioactive in dispersed rat pancreatic acini preparations. This bioactivity of CCK was completely blocked by CR 1409, a CCK-receptor antagonist. The pancreatic secretion by EVS was reduced significantly by intravenous MK-329 (formerly L364,718) to as low as 22% of control values and was completely suppressed by intravenous atropine. The increment in plasma CCK by EVS was also significantly suppressed by atropine. The present study indicates that increased pancreatic secretion by EVS is in part mediated by endogenous CCK.

Regulation of secretion of pancreatic spasmolytic polypeptide from porcine pancreas

1993 ◽  
Vol 264 (1) ◽  
pp. G22-G29
Author(s):  
T. N. Rasmussen ◽  
H. Harling ◽  
L. Thim ◽  
S. Pierzynowski ◽  
B. R. Westrom ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Hormonal Regulation ◽  
Pancreatic Enzyme ◽  
Exocrine Secretion ◽  
Total Output ◽  
Potential Growth ◽  
Porcine Pancreas ◽  
Pancreatic Enzyme Secretion ◽  
Pancreatic Exocrine ◽  
Spasmolytic Polypeptide

We studied the neural and hormonal regulation of the secretion of pancreatic spasmolytic polypeptide (PSP), a potential growth factor, from isolated perfused porcine pancreas and the pancreatic exocrine secretion of PSP in response to a meal in young conscious pigs. PSP concentrations in the pancreatic juice ranged from 1 to 180 micrograms/ml. PSP released to the venous effluent amounted to 0.4-7% of the total output. Thus PSP is predominantly an exocrine product. Electrical vagal nerve stimulation increased PSP output 30-fold. Acetylcholine mimicked the effect of nerve stimulation, which was inhibited but not abolished by atropine. Both vasoactive intestinal polypeptide and gastrin-releasing peptide stimulated PSP secretion. PSP concentration in the juice decreased in response to secretin and increased after cholecystokinin octapeptide (CCK-8), but both increased PSP output. In conscious pigs, pancreatic secretion of protein and PSP increased in parallel. Like pancreatic enzyme secretion, we conclude that PSP secretion is controlled by parasympathetic mechanisms that include both cholinergic and peptidergic pathways and by endocrine mechanisms that may include both secretin and CCK-8.

Role of pancreatic polypeptide in the regulation of pancreatic exocrine secretion in dogs

1988 ◽  
Vol 255 (5) ◽  
pp. G535-G541 ◽  
Author(s):  
K. Shiratori ◽  
K. Y. Lee ◽  
T. M. Chang ◽  
Y. H. Jo ◽  
D. H. Coy ◽  
...  
Keyword(s):  
Pancreatic Polypeptide ◽  
Pancreatic Secretion ◽  
Inhibitory Action ◽  
Peak Plasma ◽  
Peak Plasma Concentration ◽  
Exocrine Secretion ◽  
Pancreatic Exocrine Secretion ◽  
Pancreatic Exocrine ◽  
Human Pancreatic Polypeptide

The effect of intravenous infusion of synthetic human pancreatic polypeptide (HPP) or a rabbit anti-PP serum on pancreatic exocrine secretion was studied in 10 dogs with gastric and Thomas duodenal cannulas. The infusion of HPP, at a dose of 1 microgram.kg-1.h-1, achieved a plasma PP concentration that mimicked the peak plasma concentration of PP in both interdigestive and postprandial states. This dose of HPP significantly inhibited pancreatic secretion in the interdigestive state. By contrast, immunoneutralization of circulating PP by a rabbit anti-PP serum resulted in significant increases (P less than 0.05) in both interdigestive and postprandial pancreatic secretion, including water, bicarbonate, and protein. The increase in the pancreatic secretion paralleled a decrease in circulating PP level, which lasted for as long as 5 days. Furthermore, the anti-PP serum blocked the inhibitory action of exogenous HPP on pancreatic exocrine secretion. The present study indicates that endogenous PP plays a significant role in the regulation of the pancreatic exocrine secretion in both interdigestive and digestive states. Thus we conclude that PP is another hormone regulating pancreatic exocrine secretion in dogs.

Pancreatic secretory response to feeding in the calf: CCK-A receptors, but not CCK-B/gastrin receptors are involved

2000 ◽  
Vol 78 (10) ◽  
pp. 813-819 ◽  
Author(s):  
Gwenola Le Dréan ◽  
Isabelle Le Huërou-Luron ◽  
Martine Gestin ◽  
Véronique Romé ◽  
Christine Bernard ◽  
...  
Keyword(s):  
Food Intake ◽  
Pancreatic Juice ◽  
Pancreatic Secretion ◽  
Pancreatic Enzyme ◽  
Neural Pathways ◽  
Enzyme Release ◽  
Exocrine Pancreatic Secretion ◽  
External Stimuli ◽  
Bovine Species

In bovine species, as in human, the pancreas predominantly expresses cholecystokinin-B (CCK-B)/gastrin receptors. However, the role of this receptor in the regulation of meal-stimulated pancreatic enzyme release has not been determined. In milk-fed calves, we previously described prandial patterns of exocrine pancreatic secretion and a long prefeeding phase was observed. The present study was aimed at determining both the role of external stimuli in the outset of the prefeeding phase and the implication of pancreatic CCK-A and CCK-B/gastrin receptors in the mediation of pancreatic response to feeding. The first objective was studied by suppressing external stimuli associated with food intake (unexpected meal) and the second by infusing highly specific and potent antagonists of CCK-A (SR 27897) and CCK-B/gastrin (PD 135158) receptors during the prandial period. When calves were given an unexpected meal, the long prefeeding increase in pancreatic secretion was absent. SR 27897 (but not PD 135158) inhibited the preprandial phase and greatly reduced postprandial pancreatic juice and enzyme outflows. The expectancy of a meal seemed to elicit an increased pancreatic response right before a meal and CCK-A receptors may mediate this information via neural pathways. The implication of CCK and CCK-A receptors in mediating the postfeeding pancreatic response was also demonstrated. The participation of CCK-B/gastrin receptors in this regulation was not demonstrated.Key words: CCK-A and CCK-B/gastrin receptors, cholecystokinin, exocrine pancreatic secretion, feeding, milk-fed calf.

Control of interdigestive and intraduodenal meal-stimulated pancreatic secretion in rats

1990 ◽  
Vol 259 (2) ◽  
pp. G198-G204 ◽  
Author(s):  
J. Chariot ◽  
C. Nagain ◽  
F. Hugonet ◽  
A. Tsocas ◽  
C. Roze
Keyword(s):  
Pancreatic Secretion ◽  
Exocrine Secretion ◽  
Small Doses ◽  
Pancreatic Exocrine ◽  
Venous Infusion ◽  
Cck Antagonists ◽  
Protein Response ◽  
Protein Output ◽  
Cck Release

Mechanisms of neural (vagal and cholinergic) and hormonal [cholecystokinin (CCK)] control of pancreatic exocrine secretion were studied in basal interdigestive conditions and after stimulation by an intraduodenal meal in rats equipped with a semichronic pancreatic fistula. Bile was recirculated into the duodenum, and a solution of trypsin and electrolytes was continuously infused. Pancreatic secretion was compared in control experiments, after vagotomy, and after venous infusion of cholinergic and CCK antagonists. Basal pancreatic secretion was decreased by atropine, pirenzepine, and hexamethonium and to a lesser extent by vagotomy (protein output decreased more than fluid and HCO3- outputs). The CCK antagonists L364,718 and lorglumide had no effect on basal interdigestive pancreatic secretion. Small doses of atropine (8 and 25 micrograms.kg-1.h-1) did not modify the cumulated pancreatic response to the meal, whereas larger doses (75 and 225 micrograms.kg-1.h-1) increased it by 40-85%, according to the variables. Pirenzepine and hexamethonium did not modify the pancreatic response. Vagotomy had no effect on fluid and HCO3- responses and tended to increase protein response. L364,718 and lorglumide completely inhibited the protein response and decreased the fluid and HCO3- responses by 75 and 40%, respectively. L364,718 also suppressed the increased pancreatic response induced by atropine. This work confirms the prominent role of neural cholinergic mechanisms in the control of basal interdigestive pancreatic secretion in rats. In contrast, the pancreatic protein response to an intraduodenal meal depends on CCK, whereas fluid and HCO3- responses also depend on other hormonal factors. Our results suggest that a muscarinic (probably M3) mechanism can decrease the postprandial CCK release independently of the pancreatic feedback control by trypsin.

Circadian coupling between pancreatic secretion and intestinal motility in humans

2001 ◽  
Vol 280 (2) ◽  
pp. G273-G278 ◽  
Author(s):  
Jutta Keller ◽  
Gabriele Gröger ◽  
Leelamma Cherian ◽  
Britt Günther ◽  
Peter Layer
Keyword(s):  
Pancreatic Polypeptide ◽  
Pancreatic Secretion ◽  
Intestinal Motility ◽  
Plasma Concentrations ◽  
Pancreatic Enzyme ◽  
Secretory Activity ◽  
Exocrine Secretion ◽  
Motility Index ◽  
Cholinergic Tone ◽  
Pancreatic Exocrine

Human interdigestive intestinal motility follows a circadian rhythm with reduced nocturnal activity, but circadian pancreatic exocrine secretion is unknown. To determine whether circadian changes in interdigestive pancreatic secretion occur and are associated with motor events, pancreatic enzyme outputs, proximal jejunal motility, and plasma pancreatic polypeptide concentrations were measured during consecutive daytime and nighttime periods (12 h each) in seven healthy volunteers using orojejunal multilumen intubation. Studies were randomly started in the morning or evening. Nocturnally, motility decreased (motor quiescence: 67 ± 22 vs. 146 ± 37 min; motility index: 3.59 ± 0.33 vs. 2.78 ± 0.40 mmHg/min; both P < 0.05) but amylase output increased (273 ± 78 vs. 384 ± 100 U/min; P < 0.05) and protease output remained unchanged ( P > 0.05); consequently, enzyme/motility ratio increased. Amylase outputs were always lowest during phase I. Motor but not pancreatic circadian activities were associated with sleep. Pancreatic polypeptide plasma concentrations were unchanged. Consequently, intestinal motor and pancreatic exocrine functions may have different circadian rhythms, i.e., decreased motor and stable secretory activity during the night. However, the association between individual phases of interdigestive motor and secretory activity is preserved. The nocturnal increase in enzyme/motility ratio is probably not caused by increased cholinergic tone.

Plasma secretin concentrations in fasting and postprandial states in dog.

1979 ◽  
Vol 236 (5) ◽  
pp. E539 ◽  
Author(s):  
M S Kim ◽  
K Y Lee ◽  
W Y Chey
Keyword(s):  
Pancreatic Secretion ◽  
Physiological Role ◽  
Fasting State ◽  
Meat Meal ◽  
Duodenal Ph ◽  
The Mean ◽  
Bicarbonate Output ◽  
Marked Suppression ◽  
Sustained Increase

In four dogs with a modified Herrara pancreatic fistula and gastric cannula and three dogs with two duodenal cannulas, ingestion of a meat meal resulted in a significant and sustained increase in the mean plasma immunoreactive secretin concentrations, from mean fasting levels of less than 10 pg/ml to 25--55 pg/ml. This increase in the plasma secretin concentration coincided with a marked increase in pancreatic bicarbonate output and frequent decreases in the mean proximal duodenal pH to less than 4.5 from the range of 6.5 in the fasting state. Intravenous administration of cimetidine, 150 mg, produced a marked suppression of postprandial increases in both pancreatic bicarbonate output and plasma secretin concentration. Moreover, the postprandial duodenal pH rarely reached below 5.0 after cimetidine administration. These studies indicate that plasma secretin concentration does increase significantly after a meal. The postprandial increase in plasma secretin concentration appears to depend on the gastric acid delivered in the proximal duodenum. A possible physiological role of secretin in the pancreatic secretion after a meal is indicated by these findings.

Microinjection of TRH analogue into the dorsal vagal complex stimulates pancreatic secretion in rats

1995 ◽  
Vol 269 (3) ◽  
pp. G328-G334 ◽  
Author(s):  
T. Okumura ◽  
I. L. Taylor ◽  
T. N. Pappas
Keyword(s):  
Vagus Nerve ◽  
Pancreatic Secretion ◽  
Exocrine Secretion ◽  
Dependent Manner ◽  
Dorsal Vagal Complex ◽  
Pancreatic Exocrine Secretion ◽  
Pancreatic Fluid ◽  
Neurophysiological Studies ◽  
Pancreatic Exocrine ◽  
The Brain

Thyrotropin-releasing hormone (TRH) stimulates pancreatic exocrine secretion through the vagus nerve when injected into rat cerebrospinal fluid. However, little is known about the exact site of action of TRH in the brain to stimulate pancreatic secretion. Recent neuroimmunochemical and neurophysiological studies suggest that TRH could be a neurotransmitter in the dorsal vagal complex, which sends fibers to the pancreas through the vagus nerve. We therefore hypothesized that TRH may act centrally in the dorsal vagal complex to stimulate pancreatic exocrine secretion. To address this question, a TRH analogue, [1-methyl-(S)-4,5-dihydroorotyl]-L-histidyl-L-prolinamide- NH2, was microinjected into the dorsal vagal complex, and basal pancreatic fluid flow and protein secretion were measured in urethan-anesthetized rats. Microinjection of TRH analogue (0.2-2 ng/site) into the dorsal vagal complex significantly stimulated pancreatic flow and protein output in a dose-dependent manner. As a control, microinjection of the TRH analogue into the brain stem outside the vagal complex failed to stimulate pancreatic secretion. Either bilateral subdiaphragmatic vagotomy or atropine abolished the ability of the TRH analogue to stimulate pancreatic secretion. Our data suggest that TRH acts in the dorsal vagal complex to stimulate pancreatic secretion through vagus-dependent and cholinergic pathways. The dorsal vagal complex may play an important role as a central site for control of the exocrine pancreas.

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