Inhibition of pancreatic exocrine secretion via vagal afferent nerve after short-term pancreatic duct occlusion in conscious rats

1998 ◽  
Vol 114 ◽  
pp. A502
Author(s):  
S. Suzuki ◽  
S. Kanai ◽  
K. Miyasaka ◽  
A. Jimi ◽  
A. Funakoshi
2007 ◽  
Vol 293 (2) ◽  
pp. G493-G500 ◽  
Author(s):  
Eddy Viard ◽  
Zhongling Zheng ◽  
Shuxia Wan ◽  
R. Alberto Travagli

Cholecystokinin (CCK) has been proposed to act in a vagally dependent manner to increase pancreatic exocrine secretion via actions exclusively at peripheral vagal afferent fibers. Recent evidence, however, suggests the CCK-8s may also affect brain stem structures directly. We used an in vivo preparation with the aims of 1) investigating whether the actions of intraduodenal casein perfusion to increase pancreatic protein secretion also involved direct actions of CCK at the level of the brain stem and, if so, 2) determining whether, in the absence of vagal afferent inputs, CCK-8s applied to the dorsal vagal complex (DVC) can also modulate pancreatic exocrine secretion (PES). Sprague-Dawley rats (250–400 g) were anesthetized and the common bile-pancreatic duct was cannulated to collect PES. Both vagal deafferentation and pretreatment with the CCK-A antagonist lorglumide on the floor of the fourth ventricle decreased the casein-induced increase in PES output. CCK-8s microinjection (450 pmol) in the DVC significantly increased PES; the increase was larger when CCK-8s was injected in the left side of the DVC. Protein secretion returned to baseline levels within 30 min. Microinjection of CCK-8s increased PES (although to a lower extent) also in rats that underwent complete vagal deafferentation. These data indicate that, as well as activating peripheral vagal afferents, CCK-8s increases pancreatic exocrine secretion via an action in the DVC. Our data suggest that the CCK-8s-induced increases in PES are due mainly to a paracrine effect of CCK; however, a relevant portion of the effects of CCK is due also to an effect of the peptide on brain stem vagal circuits.


Pancreas ◽  
2003 ◽  
Vol 26 (1) ◽  
pp. 87-91 ◽  
Author(s):  
Kaoru Ishizaki ◽  
Shigemasa Kinbara ◽  
Makoto Kawamura ◽  
Kunio Kimura ◽  
Keiko Shiratori ◽  
...  

1998 ◽  
Vol 274 (1) ◽  
pp. G29-G34 ◽  
Author(s):  
Masao Masuda ◽  
Setsuko Kanai ◽  
Kyoko Miyasaka

We examined the role and the peripheral mechanism of action of central dopamine on basal pancreatic exocrine secretion in conscious rats. Rats were fitted with bile and pancreatic catheters to collect bile and pancreatic juice separately and also with a left lateral brain ventricle and external jugular vein catheters. After 90-min basal collection, the D1- and D2-receptor antagonists (Sch-23390 and eticlopride, respectively) and dopamine were administered into the lateral brain ventricle. Sch-23390 (30, 100, and 300 nmol/rat), but not eticlopride (300 nmol/rat), stimulated pancreatic fluid and protein secretion. Dopamine (30, 100, and 300 nmol/rat) inhibited pancreatic secretion dose dependently. Pretreatment with Sch-23390 prevented the inhibitory effect of dopamine. Intravenously injected Sch-23390 or dopamine had no effect on pancreatic secretion. The inhibitory effect of dopamine was blocked by bretylium, an inhibitor of norepinephrine release, and phentolamine, an α-blocker, but not by vagotomy. The β-antagonist propranolol alone significantly inhibited basal pancreatic secretion, and dopamine did not modify the inhibitory effect of propranolol. The proton pump inhibitor omeprazole partially but not completely reduced the inhibition by dopamine. These results suggest that central dopamine inhibits pancreatic exocrine secretion via D1-like receptors and that the inhibitory effect is mediated via sympathetic nerves, especially α-adrenoceptors.


Planta Medica ◽  
1997 ◽  
Vol 63 (05) ◽  
pp. 419-424 ◽  
Author(s):  
Ichiro Arai ◽  
Yasuhiro Komatsu ◽  
Yasuaki Hirai ◽  
Kazushi Shingu ◽  
Yoshiteru Ida ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document