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

1985 ◽  
Vol 248 (1) ◽  
pp. G110-G117 ◽  
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.

Effect of secretin and caerulein in canine pancreas: relation to prostaglandins

1983 ◽  
Vol 244 (6) ◽  
pp. G660-G667 ◽  
Author(s):  
T. Homma ◽  
K. U. Malik
Keyword(s):  
Blood Flow ◽  
Flow Rate ◽  
Exocrine Secretion ◽  
Cyclooxygenase Inhibitors ◽  
Pancreatic Exocrine Secretion ◽  
Perfused Pancreas ◽  
Pancreatic Blood Flow ◽  
Biphasic Effect ◽  
Anesthetized Dogs ◽  
Pancreatic Exocrine

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.

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

1983 ◽  
Vol 23 (10) ◽  
pp. 401-413 ◽  
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

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.

Prostaglandins: renal vascular responses to bradykinin, histamine, and nitroglycerine

1978 ◽  
Vol 234 (4) ◽  
pp. H496-H502 ◽  
Author(s):  
L. P. Feigen ◽  
B. M. Chapnick ◽  
J. E. Flemming ◽  
P. J. Kadowitz
Keyword(s):  
Blood Flow ◽  
Arachidonic Acid ◽  
Cyclooxygenase Inhibitors ◽  
Flow Probe ◽  
Vascular Responses ◽  
Vasodilator Activity ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Electromagnetic Flow Probe ◽  
Renal Vascular

A study was undertaken to evaluate the effects of inhibitors of prostaglandin (PG) synthesis on renal vascular responses to several renal vasodilators in anesthetized dogs. Indomethacin (IND) and meclofenamate (MEC), two dissimilar cyclooxygenase inhibitors were used. An electromagnetic flow probe was placed on the renal artery and a needle was inserted proximal to the probe. Injections of bradykinin, histamine, nitroglycerine, and arachidonic acid (AA) were given before and after administration of IND or MEC, 2.5 mg/kg body wt. In each experiment, inhibition of PG synthesis was estimated by reduction of vasodilator activity following AA injection. Although renal vascular resistance increased slightly after IND or MEC, elevations of renal blood flow in response to injections of bradykinin and nitroglycerine were not affected by PG synthesis inhibitors, whereas percent responses to histamine were enhanced by IND but not MEC. In addition, the action of 5 mg/kg IND on responses to injections and infusions of bradykinin was evaluated. No decrease in vasodilator activity following the kinin was detected in these studies. These results demonstrate that renal vascular responses to bradykinin, histamine, and nitroglycerine were not dependent on endogenously produced products of cyclooxygenase (e.g., prostaglandins) in the kidney of the anesthetized dog.

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.

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