Effect of neural blockades, gastrointestinal regulatory peptides, and diversion of gastroduodenal contents on periodic pancreatic secretion in the preruminant calf

1995 ◽  
Vol 73 (11) ◽  
pp. 1616-1624 ◽  
Author(s):  
R. Zabielski ◽  
P. Kiela ◽  
T. Onaga ◽  
H. Mineo ◽  
S. Kato ◽  
...  

The role of nerves, gastrointestinal peptides, and gastroduodenal contents in the regulation of pancreatic periodic function were studied in preruminant calves. Nine male, Friesian calves were surgically fitted with pancreatic and duodenal catheters, abomasal and duodenal cannulae, and duodenal electrodes. Pancreatic secretion oscillated in phase with the duodenal migrating myoelectric complex. Pancreatic secretion and duodenal motility were abolished by intravenous atropine (5 μg∙kg−1∙min−1). The frequency of pancreatic and duodenal cycles was similarly increased by motilin and decreased by pituitary adenylate cyclase activating polypeptide-27; secretin lengthened duodenal but not pancreatic cycles, resulting in loss of synchronization; cholecystokinin-8 and secretin increased pancreatic secretion (all infusions at 120 pmol∙kg−1∙h−1); intraduodenal lidocaine (2%) or diversion of gastroduodenal contents reduced pancreatic secretion without altering periodicity. In conclusion, generation of pancreatic as well as of duodenal periodicity in the calf depends upon cholinergic neural efferent input. Secretin, cholecystokinin-8, pituitary adenylate cyclase activating polypeptide, duodenal contents, and mucosal afferent receptors seem to have relatively minor regulatory roles but can modulate the level of pancreatic secretion. The importance of enteric neural influence from the duodenum and the role of motilin in the regulation of pancreatic periodicity and its synchronization with the duodenal motility cycle remain to be determined.Key words: pancreatic juice, duodenal migrating myoelectric complex, secretin, motilin, pituitary adenylate cyclase activating polypeptide, atropine, lidocaine, calf.

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Rubina Marzagalli ◽  
Soraya Scuderi ◽  
Filippo Drago ◽  
James A. Waschek ◽  
Alessandro Castorina

Enduring diabetes increases the probability of developing secondary damage to numerous systems, and these complications represent a cause of morbidity and mortality. Establishing the causes of diabetes remains the key step to eradicate the disease, but prevention as well as finding therapies to ameliorate some of the major diabetic complications is an equally important step to increase life expectancy and quality for the millions of individuals already affected by the disease or who are likely to develop it before cures become routinely available. In this review, we will firstly summarize some of the major complications of diabetes, including endothelial and pancreatic islets dysfunction, retinopathy, and nephropathy, and then discuss the emerging roles exerted by the neuropeptide pituitary adenylate cyclase activating polypeptide (PACAP) to counteract these ranges of pathologies that are precipitated by the prolonged hyperglycemic state. Finally, we will describe the main signalling routes activated by the peptide and propose possible future directions to focus on developing more effective peptide-based therapies to treat the major complications associated with longstanding diabetes.


1996 ◽  
Vol 149 (2) ◽  
pp. 287-295 ◽  
Author(s):  
C S Kovacs ◽  
C L Chik ◽  
B Li ◽  
E Karpinski ◽  
A K Ho

Abstract Pituitary adenylate cyclase-activating peptide (PACAP) and vasoactive intestinal peptide (VIP) share 68% homology and function as neurotransmitters or neuroendocrine factors. Although VIP immunoreactivity has been detected in bone cells, the presence of PACAP or PACAP receptors in bone has not been determined. In this study, we investigated the role of PACAP and VIP in regulating cAMP accumulation in the UMR 106 osteoblast-like tumor cell line. PACAP 27 (10−9 to 3 × 10−7 m), PACAP 38 (10−9 to 3 × 10−7 m) and VIP (10−8 to 10−6 m) stimulated cAMP accumulation up to eightfold. PACAP 27 was slightly more potent than PACAP 38, and both were tenfold more potent than VIP. Both PACAP- and VIP-stimulated cAMP accumulation were potentiated by 4β-phorbol 12-myristate 13-acetate, an activator of protein kinase C. Two PACAP antagonists, PACAP 6–27 (3 × 10−6 m) and PACAP 6–38 (3 × 10−6 m), blocked PACAP- and VIP-stimulated cAMP accumulation. Two VIP antagonists ([Lys1,Pro2,5,Arg3,4,Tyr6]-VIP, and 4 Cl-d-Phe6,Leu17]-VIP) did not reduce the PACAP-or VIP-stimulated cAMP accumulation. Pretreatment with PACAP 27, PACAP 38 or VIP equally blocked PACAP- and VIP-stimulated cAMP accumulation. These results suggest that PACAP is a more potent stimulator of cAMP accumulation than VIP in UMR 106 cells. PACAP and VIP may share a role in the paracrine or neuroendocrine regulation of bone metabolism. Journal of Endocrinology (1996) 149, 287–295


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