The Effect of Pancreatic Polypeptide and Peptide YY on Pancreatic Blood Flow and Pancreatic Exocrine Secretion in the Anesthetized Dog

We investigated the effect of secretin and caerulein on pancreatic circulation and exocrine secretion and its relation to prostaglandin (PG) synthesis by studying the effect of these peptides on the pancreatic blood flow and the flow rate of pancreatic exocrine secretion in the isolated blood-perfused pancreas of pentobarbital-anesthetized dogs without or with pretreatment with the cyclooxygenase inhibitors, indomethacin and meclofenamate. Intra-arterial administration of secretin (0.1–0.3 U/kg) produced an initial vasoconstriction followed by vasodilation. On the other hand, caerulein (50–200 ng/kg) produced vasodilation and increased pancreatic blood flow in a dose-related manner. Both secretin and caerulein increased the flow rate of pancreatic exocrine secretion. In animals pretreated with either indomethacin or meclofenamate, the ability of secretin to produce an initial vasoconstriction was abolished and the subsequent vasodilator component of the response as well as caerulein-induced vasodilation were reduced in duration. The effect of caerulein but not of secretin to stimulate the flow rate of pancreatic exocrine secretion was reduced by indomethacin and meclofenamate. Administration of PGI2 and PGE2 into the pancreas caused vasodilation, whereas PGF2 alpha and PGD2 produced a biphasic effect, i.e., an initial vasoconstriction followed by vasodilation. Infusion of either PGI2 or PGE2 but not that of PGF2 alpha or PGD2 minimized the effect of cyclooxygenase inhibitors to reduce the duration of vasodilator response elicited by secretin and caerulein. Prostaglandins neither altered the basal nor the rise in flow rate of pancreatic exocrine secretion produced by secretin and caerulein. These data indicate that in the canine pancreas prostaglandins contribute to the effects of secretin and caerulein to increase pancreatic blood flow but not to their effect on pancreatic exocrine secretion.

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A vasopressin-induced decrease in pancreatic blood flow and in pancreatic exocrine secretion in the anesthetized dog

Pflügers Archiv - European Journal of Physiology ◽

10.1007/bf00581567 ◽

1984 ◽

Vol 400 (3) ◽

pp. 324-328 ◽

Cited By ~ 12

Author(s):

H. J. M. Beijer ◽

A. H. J. Maas ◽

G. A. Charbon

Keyword(s):

Blood Flow ◽

Exocrine Secretion ◽

Pancreatic Exocrine Secretion ◽

Pancreatic Blood Flow ◽

Pancreatic Exocrine

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Contribution of prostaglandins to dopamine actions in the pancreas of anesthetized dogs

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1985.248.1.g110 ◽

1985 ◽

Vol 248 (1) ◽

pp. G110-G117 ◽

Cited By ~ 1

Author(s):

K. Iwatsuki ◽

T. Homma ◽

K. U. Malik

Keyword(s):

Blood Flow ◽

Arachidonic Acid ◽

Flow Rate ◽

Inhibitory Effect ◽

Exocrine Secretion ◽

Cyclooxygenase Inhibitors ◽

Pancreatic Exocrine Secretion ◽

Pancreatic Blood Flow ◽

Anesthetized Dogs ◽

Pancreatic Exocrine

We investigated the effect of dopamine and arachidonic acid on pancreatic blood flow and exocrine secretion in the isolated blood-perfused pancreas of pentobarbital sodium-anesthetized dogs without or with pretreatment with indomethacin or sodium meclofenamate in the absence and during infusion of prostaglandins I2 or E2 (PGI2 or PGE2). Intra-arterial administration of dopamine (50-500 ng/kg) produced an initial vasoconstriction followed by vasodilation and enhanced flow rate of pancreatic exocrine secretion. Arachidonic acid (0.5-5 micrograms/kg) produced vasodilation without altering the flow rate of pancreatic exocrine secretion. In animals pretreated with indomethacin or sodium meclofenamate (10 mg/kg iv), the magnitude and the duration of the biphasic vascular response but not the increase in flow rate of pancreatic exocrine secretion elicited by dopamine were reduced. Arachidonic acid-induced vasodilation was abolished by the cyclooxygenase inhibitors. During infusion of PGI2 or PGE2 (10 ng X kg-1 X min-1 ia), the inhibitory effect of indomethacin or sodium meclofenamate on the vasodilator phase of the response to dopamine was diminished. These data suggest that prostaglandins, presumably PGI2 and PGE2, contribute to the effect of dopamine to increase pancreatic blood flow but not to increase pancreatic exocrine secretion in anesthetized dogs.

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Effects of Furosemide on Biliary Secretion, Pancreatic Blood Flow, and Pancreatic Exocrine Secretion

The Journal of Clinical Pharmacology ◽

10.1002/j.1552-4604.1983.tb01783.x ◽

1983 ◽

Vol 23 (10) ◽

pp. 401-413 ◽

Cited By ~ 7

Author(s):

STANLEY WALLACH ◽

GERARD A. CHARBON ◽

HEIN J. M. BEIJER ◽

HERMAN J. ENDEMAN ◽

J. ODO O. HOEKE ◽

...

Keyword(s):

Blood Flow ◽

Exocrine Secretion ◽

Biliary Secretion ◽

Pancreatic Exocrine Secretion ◽

Pancreatic Blood Flow ◽

Pancreatic Exocrine

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Structural requirements of peptide YY for biological activity at enteric sites

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1992.263.5.g695 ◽

1992 ◽

Vol 263 (5) ◽

pp. G695-G701 ◽

Cited By ~ 1

Author(s):

K. Yoshinaga ◽

T. Mochizuki ◽

N. Yanaihara ◽

K. Oshima ◽

M. Izukura ◽

...

Keyword(s):

Insulin Secretion ◽

Acid Secretion ◽

Gastric Acid Secretion ◽

Gastric Acid ◽

Insulin Release ◽

Peptide Yy ◽

Exocrine Secretion ◽

Pancreatic Exocrine Secretion ◽

Structural Requirements ◽

Pancreatic Exocrine

Peptide YY (PYY) is a colonic hormone consisting of 36 amino acids that is a potent inhibitor of pancreatic exocrine, gastric acid, and insulin secretion. The objective of the present experiments was to characterize the structural requirements of PYY for inhibition of pancreatic exocrine, gastric acid, and insulin secretion, using conscious dogs prepared with gastric and pancreatic fistulas. Intravenous administration of PYY-(1-36), PYY-(3-36), or PYY-(4-36) (400 pmol.kg-1 x h-1) inhibited cholecystokinin-8-stimulated (25 pmol.kg-1 x h-1) pancreatic exocrine secretion (P < 0.05); however, PYY-(1-10), PYY-(1-20), PYY-(6-36), PYY-(10-36), PYY-(13-36), PYY-(24-36), and PYY-(27-36) did not inhibit pancreatic exocrine secretion. Intravenous administration of PYY-(1-36), PYY-(3-36), or PYY-(4-36) (200, 400, 800 pmol.kg-1 x h-1) inhibited pentagastrin (0.5 microgram.kg-1 x h-1)-stimulated gastric acid secretion (P < 0.05), as well as 2-deoxy-D-glucose-stimulated insulin release (75 mg/kg) in a dose-related manner. PYY-(6-36), PYY-(13-36), and [Leu31, Pro34] neuropeptide Y did not inhibit either gastric acid secretion or insulin release. In the gastric acid and insulin secretion bioassays, PYY-(1-36) was significantly more potent than PYY-(3-36) and PYY-(4-36); however, in the pancreatic exocrine secretion bioassay, the inhibitory effects of PYY-(3-36) and PYY-(1-36) did not differ significantly. PYY-(4-36) was less potent than PYY-(1-36) on pancreatic exocrine secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

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Cholecystokinin-8s excites identified rat pancreatic-projecting vagal motoneurons

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00116.2007 ◽

2007 ◽

Vol 293 (2) ◽

pp. G484-G492 ◽

Cited By ~ 22

Author(s):

Shuxia Wan ◽

F. Holly Coleman ◽

R. Alberto Travagli

Keyword(s):

Brain Stem ◽

Pancreatic Polypeptide ◽

Potassium Conductance ◽

Input Resistance ◽

Exocrine Secretion ◽

Motor Nucleus ◽

Pancreatic Exocrine Secretion ◽

Calcium Dependent ◽

Synaptic Circuits ◽

Pancreatic Exocrine

It is known that cholecystokinin (CCK) acts in a paracrine fashion to increase pancreatic exocrine secretion via vagal circuits. Recent evidence, however, suggests that CCK-8s actions are not restricted to afferent vagal fibers, but also affect brain stem structures directly. Within the brain stem, preganglionic neurons of the dorsal motor nucleus of the vagus (DMV) send efferent fibers to subdiaphragmatic viscera, including the pancreas. Our aims were to investigate whether DMV neurons responded to exogenously applied CCK-8s and, if so, the mechanism of action. Using whole cell patch-clamp recordings we show that perfusion with CCK-8s induced a concentration-dependent excitation in ∼60% of identified pancreas-projecting DMV neurons. The depolarization was significantly reduced by tetrodotoxin, suggesting both direct (on the DMV membrane) and indirect (on local synaptic circuits) effects. Indeed, CCK-8s increased the frequency of miniature excitatory currents onto DMV neurons. The CCK-A antagonist, lorglumide, prevented the CCK-8s-mediated excitation whereas the CCK-B preferring agonist, CCK-nonsulfated, had no effect, suggesting the involvement of CCK-A receptors only. In voltage clamp, the CCK-8s-induced inward current reversed at −106 ± 3 mV and the input resistance increased by 150 ± 15%, suggesting an effect mediated by the closure of a potassium conductance. Indeed, CCK-8s reduced both the amplitude and the time constant of decay of a calcium-dependent potassium conductance. When tested with pancreatic polypeptide (which reduces pancreatic exocrine secretion), cells that responded to CCK-8s with an excitation were, instead, inhibited by pancreatic polypeptide. These data indicate that CCK-8s may control pancreas-exocrine secretion also via an effect on pancreas-projecting DMV neurons.

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