Insulin Inhibits Secretin-Induced Pancreatic Bicarbonate Output Via Cholinergic Mechanisms

Pancreas ◽  
2002 ◽  
Vol 24 (4) ◽  
pp. 380-385 ◽  
Author(s):  
Marissa Howard-McNatt ◽  
Timothy Simon ◽  
Yuanhong Wang ◽  
Aaron S. Fink
1987 ◽  
Vol 252 (6) ◽  
pp. G755-G761 ◽  
Author(s):  
J. Chariot ◽  
J. de la Tour ◽  
P. Anglade ◽  
C. Roze

Extrinsic denervations of the pancreas were carried out in rats using bilateral truncal abdominal vagotomy and/or celiac and superior mesenteric ganglionectomy. Chronic fistulas were produced and pancreatic secretion was then measured in conscious animals. In all three groups of extrinsically denervated animals the basal pancreatic secretion was significantly decreased by 15-44% (fluid), 32-59% (bicarbonate output), and 33-43% (protein output). Meal-stimulated secretion was decreased in denervated animals by 38-57% (fluid), 32-44% (bicarbonate output), and 36-64% (protein output). In extrinsically denervated rats, atropine inhibited basal pancreatic fluid by 26-38%, bicarbonate output by 46-71%, and protein output by 63-80%, whereas hexamethonium inhibited basal protein output by 36-58%. These data indicate that cholinergic mechanisms persist in the pancreas after extrinsic denervation. This may correspond either to the spontaneous activity of intrapancreatic excitatory cholinergic neurons or to the drive of these neurons by preganglionic fibers running through nonclassic (such as duodenopancreatic) pathways. No important difference was observed between the effects of vagotomy and those of celiac and superior mesenteric ganglionectomy, indicating that most of the excitatory vagal fibers for the exocrine pancreas run through the celiac pathway and that adrenergic fibers had little effect on the conditions tested.


2021 ◽  
Author(s):  
Noah A. Omeiza ◽  
Halimat A. Abdulrahim ◽  
Abdullateef I. Alagbonsi ◽  
Precious U. Ezurike ◽  
Talha K. Soluoku ◽  
...  

1988 ◽  
Vol 43 (4) ◽  
pp. 507-514 ◽  
Author(s):  
L.S. Kaufman ◽  
B.S. McEwen ◽  
D.W. Pfaff

1996 ◽  
Vol 9 (12) ◽  
pp. 2468-2473 ◽  
Author(s):  
K. Matsumoto ◽  
H. A Izawa ◽  
H. Inoue ◽  
S. Takata ◽  
M. Shigyo ◽  
...  

2011 ◽  
Vol 31 (6) ◽  
pp. 606-616 ◽  
Author(s):  
Madhu Lata Sankhwar ◽  
Rajesh S Yadav ◽  
Rajendra K Shukla ◽  
Aditya B Pant ◽  
Dhirendra Singh ◽  
...  

Studies on the neurobehavioral toxicity of monocrotophos, an organophosphate, have been carried out on rats following their exposure from postnatal day (PD) 22 to PD 49 to investigate whether neurobehavioral changes are transient or persistent. Exposure of rats to monocrotophos (0.50 or 1.0 mg/kg body weight, p.o.) decreased body weight (10% and 30%) and impaired grip strength (28% and 32%) and learning ability (65% and 68%) at both the doses, respectively in comparison to controls. A trend of recovery was observed in body weight and learning, while decrease in grip strength persisted in rats 15 days after withdrawal. Activity of acetylcholinesterase was decreased in frontal cortex (36% and 67%), hippocampus (21% and 49%) and cerebellum (29% and 51%) in monocrotophos-treated rats at both the doses. The decrease in the activity of acetylcholinesterase persisted in frontal cortex and hippocampus; however, a trend of recovery was observed in cerebellum 15 days after withdrawal. Binding of 3 H-quinuclidinyl benzilate ( 3 H-QNB) to frontocortical (19% and 35%), hippocampal (32% and 39%) and cerebellar (19% and 28%) membranes was decreased in monocrotophos-treated rats compared to controls. The decrease in the binding of 3 H-QNB persisted in frontocortical, hippocampal and cerebellar membranes 15 days after withdrawal. The results suggest that repeated exposure to monocrotophos in rats may cause behavioral and neurochemical modifications which may persist even after withdrawal. The findings are of concern in view of the high consumption of monocrotophos in many countries.


1979 ◽  
Vol 236 (5) ◽  
pp. E539 ◽  
Author(s):  
M S Kim ◽  
K Y Lee ◽  
W Y Chey

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.


2017 ◽  
Vol 142 ◽  
pp. 3-6 ◽  
Author(s):  
Marco A.M. Prado ◽  
Pascale Marchot ◽  
Israel Silman

2000 ◽  
Vol 118 (4) ◽  
pp. A618
Author(s):  
Brent Harris ◽  
Satish SC Rao ◽  
Bruce Brown ◽  
Vani Vernuri ◽  
Konrad Schulze

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