Inhibitory effect of central dopamine on basal pancreatic secretion in conscious rats

1998 ◽  
Vol 274 (1) ◽  
pp. G29-G34 ◽  
Author(s):  
Masao Masuda ◽  
Setsuko Kanai ◽  
Kyoko Miyasaka
Keyword(s):  
Pancreatic Secretion ◽  
Sch 23390 ◽  
Sympathetic Nerves ◽  
Inhibitory Effect ◽  
Exocrine Secretion ◽  
External Jugular Vein ◽  
Pancreatic Exocrine Secretion ◽  
Conscious Rats ◽  
Brain Ventricle ◽  
Pancreatic Exocrine

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.

scholarly journals MEK inhibits secretin release and pancreatic secretion: roles of secretin-releasing peptide and somatostatin

2001 ◽  
Vol 280 (5) ◽  
pp. G890-G896 ◽  
Author(s):  
James P. Li ◽  
Kae Yol Lee ◽  
Ta-Min Chang ◽  
William Y. Chey
Keyword(s):  
Pancreatic Secretion ◽  
Inhibitory Effect ◽  
Exocrine Secretion ◽  
Rabbit Serum ◽  
Normal Rabbit Serum ◽  
Pancreatic Exocrine Secretion ◽  
Pancreatic Fluid ◽  
Pancreatic Exocrine ◽  
Small Intestinal ◽  
Secretin Release

We investigated the mechanism of action of methionine enkephalin (MEK) on HCl-stimulated secretin release and pancreatic exocrine secretion. Anesthetized rats with pancreatobiliary cannulas and isolated upper small intestinal loops were perfused intraduodenally with 0.01 N HCl while bile and pancreatic juice were diverted. The effect of intravenous MEK on acid-stimulated secretin release and pancreatic exocrine secretion was then studied with or without coinfusion of naloxone, an anti-somatostatin (SS) serum, or normal rabbit serum. Duodenal acid perfusate, which contains secretin-releasing peptide (SRP) activity, was collected from donor rats with or without pretreatment with MEK, MEK + naloxone, or MEK + anti-SS serum, concentrated by ultrafiltration, and neutralized. The concentrated acid perfusate (CAP), which contains SRP bioactivity, was infused intraduodenally into recipient rats. MEK increased plasma SS concentration and inhibited secretin release and pancreatic fluid and bicarbonate secretion dose-dependently. The inhibition was partially reversed by naloxone and anti-SS serum but not by normal rabbit serum. In recipient rats, CAP increased plasma secretin level and pancreatic secretion. CAP SRP bioactivity decreased when it was collected from MEK-treated donor rats; this was partially reversed by coinfusion with naloxone or anti-SS serum. These results suggest that in the rat, MEK inhibition of acid-stimulated pancreatic secretion and secretin release involves suppression of SRP activity release. Thus the MEK inhibitory effect appears to be mediated in part by endogenous SS.

Effect of [(CH2NH)4,5]secretin on pancreatic exocrine secretion in guinea pigs and rats

1993 ◽  
Vol 265 (5) ◽  
pp. G805-G810 ◽  
Author(s):  
C. D. Kim ◽  
P. Li ◽  
K. Y. Lee ◽  
D. H. Coy ◽  
W. Y. Chey
Keyword(s):  
Pancreatic Secretion ◽  
Guinea Pigs ◽  
Partial Agonist ◽  
Inhibitory Effect ◽  
Exocrine Secretion ◽  
Pancreatic Exocrine Secretion ◽  
Pancreatic Acini ◽  
Secretin Receptor ◽  
Pancreatic Exocrine

[psi 4,5]Secretin was shown to be a secretin receptor antagonist that inhibits secretin-stimulated increase in adenosine 3',5'-cyclic monophosphate in isolated pancreatic acini of the guinea pig. To determine whether it inhibits pancreatic exocrine secretion in vivo, we have studied the effect of [psi 4,5]secretin on the pancreatic secretion stimulated by secretin in anesthetized guinea pigs and rats. In basal state, [psi 4,5]secretin given intravenously for 2 or 3 h in varying doses of 1.6-32.7 nmol.kg-1.h-1 dose dependently increased pancreatic secretion of both fluid and bicarbonate during the 1st h, but it returned gradually to basal level within 2 or 3 h. On the other hand, [psi 4,5]secretin significantly inhibited the pancreatic secretion stimulated by either exogenous or endogenous secretin in a dose-related manner. The inhibitory effect of [psi 4,5]secretin in guinea pigs was greater than that in rats. However, it did not completely block the secretin-stimulated pancreatic secretion, whereas a rabbit antisecretin serum suppressed it completely. We conclude that 1) in the unstimulated state, [psi 4,5]secretin is a partial agonist of pancreatic exocrine secretion of both fluid and bicarbonate; and 2) when pancreatic secretion is stimulated by secretin, unlike an antisecretin serum, it is a partial inhibitor in intact guinea pigs and rats.

Roles of 5-HT receptors in the release and action of secretin on pancreatic secretion in rats

2001 ◽  
Vol 280 (4) ◽  
pp. G595-G602 ◽  
Author(s):  
James P. Li ◽  
Ta-Min Chang ◽  
William Y. Chey
Keyword(s):  
Receptor Antagonist ◽  
Pancreatic Secretion ◽  
Inhibitory Effect ◽  
Exocrine Secretion ◽  
Pancreatic Exocrine Secretion ◽  
Receptor Antagonists ◽  
Duodenal Acidification ◽  
Cholinergic Pathway ◽  
Inhibited Acid ◽  
Pancreatic Exocrine

5-Hydroxytryptamine (serotonin, 5-HT) is a hormone and neurotransmitter regulating gastrointestinal functions. 5-HT receptors are widely distributed in gastrointestinal mucosa and the enteric nervous system. Duodenal acidification stimulates not only the release of both 5-HT and secretin but also pancreatic exocrine secretion. We investigated the effect of 5-HT receptor antagonists on the release of secretin and pancreatic secretion of water and bicarbonate induced by duodenal acidification in anesthetized rats. Both the 5-HT2 receptor antagonist ketanserin and the 5-HT3 receptor antagonist ondansetron at 1–100 μg/kg dose-dependently inhibited acid-induced increases in plasma secretin concentration and pancreatic exocrine secretion. Neither the 5-HT1 receptor antagonists pindolol and 5-HTP-DP nor the 5-HT4 receptor antagonist SDZ-205,557 affected acid-evoked release of secretin or pancreatic secretion. None of the 5-HT receptor antagonists affected basal pancreatic secretion or plasma secretin concentration. Ketanserin or ondansetron at 10 μg/kg or a combination of both suppressed the pancreatic secretion in response to intravenous secretin at 2.5 and 5 pmol · kg−1 · h−1 by 55–75%, but not at 10 pmol · kg−1 · h−1. Atropine (50 μg/kg) significantly attenuated the inhibitory effect of ketanserin on pancreatic secretion but not on the release of secretin. These observations suggest that 5-HT2 and 5-HT3receptors mediate duodenal acidification-induced release of secretin and pancreatic secretion of fluid and bicarbonate. Also, regulation of pancreatic exocrine secretion through 5-HT2 receptors may involve a cholinergic pathway in the rat.

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.

Effect of Cholecystokinin1 Receptor Antagonist Loxiglumide (CR1505) on Basal Pancreatic Exocrine Secretion in Conscious Rats

Pancreas ◽  
2003 ◽  
Vol 26 (1) ◽  
pp. 87-91 ◽  
Author(s):  
Kaoru Ishizaki ◽  
Shigemasa Kinbara ◽  
Makoto Kawamura ◽  
Kunio Kimura ◽  
Keiko Shiratori ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Exocrine Secretion ◽  
Pancreatic Exocrine Secretion ◽  
Conscious Rats ◽  
Pancreatic Exocrine

Effect of ACh and calmodulin inhibitor on O2 transfer from exocrine pancreatic microvessels of rats

1996 ◽  
Vol 271 (1) ◽  
pp. H1-H7 ◽  
Author(s):  
A. Seiyama ◽  
H. Kosaka ◽  
T. Shiga
Keyword(s):  
Pancreatic Secretion ◽  
Binding Protein ◽  
Control Level ◽  
Exocrine Secretion ◽  
The Other ◽  
Pancreatic Exocrine Secretion ◽  
O2 Extraction ◽  
Pancreatic Exocrine ◽  
O2 Transfer ◽  
Krebs Henseleit Buffer

Effects of acetylcholine (ACh) and calmodulin (CaM) inhibitor, N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide hydrochloride (W-7), on the rate of O2 release (Ro2) from single exocrine pancreatic microvessels of anesthetized rats were investigated with dual-spot microspectroscopy. The surface of the pancreas was superfused with Krebs-Henseleit buffer containing various concentrations of ACh and/or W-7. Superfusion of ACh (> or = 20 microM) elevated Ro2 as well as pancreatic secretion approximately 2.5 times higher than that of control level, whereas superfusion of W-7 (> or = 100 microM) reduced approximately 50%. In both cases, O2 inflow in single microvessels, as quantified by oxyhemoglobin inflow into the microvessels, was maintained at control level. On the other hand, superfusion of both ACh and W-7 did not modify Ro2 and pancreatic secretion, despite significant reduction in O2 inflow. These results indicate that 1) the ACh-induced elevation of O2 release from single microvessels is accomplished by increased O2 extraction instead of increased O2 inflow in the microvessels, and 2) the activity of a W-7-sensitive Ca2+ binding protein, most likely CaM, is responsible for half of the microvascular O2 transfer and of the pancreatic exocrine secretion.

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