Exocrine Secretion In Rats Research Articles

Central secretin mediates pancreatic exocrine secretion in rats

Central secretin mediates pancreatic exocrine secretion in rats

Guanidinated casein hydrolysate stimulation of cholecystokinin release via pancreatic enzyme- and cholinergic-independent mechanisms in rats.

We had demonstrated that a peptic hydrolysate of guanidinated casein that is made from casein by the conversion of lysine to homoarginine stimulated pancreatic exocrine secretion in rats with chronic bile-pancreatic juice (BPJ) diversion from the proximal small intestine. This modified protein also stimulated cholecystokinin (CCK) release from dispersed rat intestinal cells. In this study, we found that guanidinated casein hydrolysate stimulates CCK release in chronic BPJ-diverted rats with cholinergic control blocked by atropine. Intraduodenal guanidinated casein hydrolysate increased portal plasma CCK concentration and pancreatic secretion in atropine-treated BPJ-diverted rats. In contrast, the portal plasma CCK concentration was not increased by intact casein hydrolysate. We conclude that guanidinated casein hydrolysate directly stimulates CCK release from the intestine via some cholinergic-independent mechanism, and an increase of the pancreatic exocrine secretion is regulated by CCK released by guanidinated casein hydrolysate. A guanidyl residue is likely to be involved in this control.

P–349 - Site of action of cholecystokinin antagonist CR1505 on pancreatic exocrine secretion in rats

P–349 - Site of action of cholecystokinin antagonist CR1505 on pancreatic exocrine secretion in rats

Physiological role of nitric oxide in the regulation of pancreatic exocrine secretion in rats

Physiological role of nitric oxide in the regulation of pancreatic exocrine secretion in rats

Stimulatory effects of the central amygdaloid nucleus on pancreatic exocrine secretion in rats

The effects of electrical stimulation of the central (CE) and basolateral (BL) amygdaloid nuclei on pancreatic exocrine secretion were tested in urethane-anesthetized rats. Electrical stimulation (0.1 mA, 1 ms, 40 Hz) of the CE significantly increased basal and hormone (secretin+cholecystokinin-8)-infused pancreatic exocrine secretion. These increases in pancreatic secretion were abolished by bilateral vagotomy. Electrical stimulation of the BL had no significant effect on basal and hormone-infused secretion. We conclude that the CE plays a stimulatory role in pancreatic exocrine secretion via the vagus nerve but the BL does not affect pancreatic secretion.

A physiological role of peptide YY on exocrine pancreatic secretion in rats

Background: Peptide YY (PYY) given intravenously was shown to inhibit pancreatic exocrine secretion both in the dog and the rat. However, a possible physiological role of PYY on the pancreatic secretion has not been clarified. The present study was undertaken to investigate its physiological role on the exocrine pancreas. Methods: In conscious rats, plasma PYY was determined in response to oral ingestion of a 6-mL meal and intravenous infusion of PYY; small intestinal transit time was measured by phenol red as a nonabsorbable marker, and pancreatic secretory studies were performed in rats with pancreatic fistulas and jugular vein catheters. Results: Oral ingestion of the meal (containing phenol red, 1.6 mg/100 mL) significantly increased plasma PYY within 30 minutes. During this period, most (97%) of the phenol red was detected in the proximal two-thirds of the small intestine. Intravenous infusion of PYY in 25, 50, and 100 pmol · kg−1 · h−1 produced a dose-dependent increase in plasma PYY. The dose of PYY that simulated the peak postprandial level was 50 pmol · kg−1 · h−1, and this dose of PYY significantly inhibited the pancreatic secretion stimulated by physiological doses of secretin and cholecystokinin-8 (CCK-8). After the meal, pancreatic secretion of bicarbonate and protein significantly increased in rats pretreated with normal rabbit serum, whereas this increase was significantly augmented in rats pretreated with an anti-PYY serum because the postprandial increase in plasma PYY was abolished. Conclusions: PYY plays a regulatory role in the postprandial pancreatic exocrine secretion in rats.

Effect of Ethanol on Pancreatic Exocrine Secretion in Rats

The effect of ethanol on pancreatic exocrine secretion was studied in isolated rat pancreatic acini. Ethanol caused a dose-dependent stimulation of amylase release, and a twofold increase of amylase release was observed with 600 mM ethanol. Ethanol inhibited cholecystokinin octapeptide (CCK-8)- and carbamylcholine-stimulated amylase release and similarly inhibited binding of [125I]CCK-8 and [N-methyl-3H]scopolamine to isolated rat pancreatic acini in a dose-dependent manner. The inhibitory effect of ethanol was fully reversible with respect to CCK-8-induced amylase release. On the other hand, ethanol potentiated secretin- and vasoactive intestinal peptide (VIP)-stimulated amylase release. Ethanol induced a small but significant increase in Ca2+ efflux, whereas CCK-8 induced an immediate and large increase, but ethanol significantly inhibited CCK-8-stimulated Ca2+ efflux. The present study clearly demonstrates the dual effects of ethanol on pancreatic exocrine function: stimulation and inhibition. We suggest that mobilization of intracellular Ca2+ may be involved in the mechanism of ethanol's action on isolated rat pancreatic acini.

Effects of MCI-727, a New Anti-Ulcer Agent, on Plasma Secretin Concentration in Rats and Dogs and Pancreatic Exocrine Secretion in Rats.

In the present study, we investigated the effects of MCI-727, a new anti-ulcer agent, on plasma immunoreactive secretin concentration in rats and dogs using secretin specific RIA with the ethanol extraction method. Plasma secretin levels were increased dose-dependently 10 min after oral administration of MCI-727 in rats (control: 5.5 +/- 0.6; MCI-727, 10 mg/kg: 10.4 +/- 2.6; 30 mg/kg: 15.3 +/- 1.5; 100 mg/kg: 20.7 +/- 2.6 pg/ml, n = 6). Teprenone also caused a significant increase of plasma secretin at 10 min after oral administration at the doses of 30, 100 and 300 mg/kg. Under the same conditions, MCI-727 and teprenone did not alter the plasma immunoreactive gastrin concentration in rats. From the results of the time course study, the increasing effect of MCI-727 (30 mg/kg, p.o.) on plasma secretin remained for at least 240 min after administration. On the other hand, the increasing effect of teprenone (200 mg/kg, p.o.) was only observed at 30 and 60 min after administration. Furthermore, MCI-727 had increasing effects on plasma secretin concentration in dogs, but teprenone had no effects in this species. The volume of pancreatic secretion and the pancreatic bicarbonate output increased after intra-duodenal administration of MCI-727 at 30 and 100 mg/kg in rats. Similar effects were also observed with teprenone (30-300 mg/kg, i.d.) or secretin (Secrepan, 0.1-1.0 unit/kg, i.v.).

Effects of MCI-727, a New Anti-Ulcer Agent, on Plasma Secretin Concentration in Rats and Dogs and Pancreatic Exocrine Secretion in Rats

Effects of MCI-727, a New Anti-Ulcer Agent, on Plasma Secretin Concentration in Rats and Dogs and Pancreatic Exocrine Secretion in Rats

Inhibitory effect of CR 1409 (Cholecystokinin Antagonist) on pancreatic exocrine secretion in rats

Inhibitory effect of CR 1409 (Cholecystokinin Antagonist) on pancreatic exocrine secretion in rats

Effects of cisapride on the pancreatic exocrine secretion in rats.

Exocrine pancreatic secretion to intravenous injections of a new stimulant of gastrointestinal motility, R51,619 (cisapride) was studied in conscious rats, and in the isolated pancreatic acini in vitro. The injection of cisapride (2 mg/kg) significantly increased fluid, bicarbonate and protein output in vivo. Atropine completely abolished the pancreatic responses to cisapride, and CR 1409, a new glutaramic acid derivative and a competitive cholecystokinin (CCK) inhibitor, tended to decrease the cisapride-induced pancreatic exocrine secretion. However, amylase release and Ca2+ efflux from the isolated pancreatic acini were not stimulated. These results suggest that cisapride indirectly affects the pancreatic exocrine secretion primarily by releasing acethycholine from the intrapancreatic nerve endings and in part by releasing CCK from the duodenum, but has no direct action on the pancreas.

Neurotensin stimulates pancreatic exocrine secretion in rats

Neurotensin (NT) stimulates pancreatic exocrine secretion in dogs and humans. The purpose of this study was to examine the effect of exogenous neurotensin on pancreatic exocrine secretion in rats. Five Sprague-Dawley male rats were prepared with pancreatic, gastric and duodenal fistulas. Bile was shunted into the duodenum in order to collect pure pancreatic juice. 24 h later, neurotensin (0.05, 0.1, 0.2, 0.3, 1.0 nmol/kg) was infused intravenously in a random fashion. Pancreatic juice was collected every 10 min, and the volume was recorded and protein and bicarbonate were measured. Neurotensin stimulated, in a dose-related manner, the pancreatic secretion of water, protein and bicarbonate. Neurotensin may be involved in the physiologic control of pancreatic secretion in rats.

Etorphine inhibition of pancreatic exocrine secretion in rats: Comparison with methadone

The effects of etorphine, a potent opiate agonist without preferential affinity for μ, δ or κ receptors, on exocrine pancreatic secretion were studied in rats fitted with chronic or acute pancreatic fistulas and compared to those of methadone, a well-documented μ agonist. In conscious rats etorphine (3 μg/kg s.c.) inhibited basal pancreatic secretion by about 50% for volume and bicarbonate output and by 70% for protein output. Pancreatic secretion returned to its basal level within 2 h. Methadone (5 kg/mg s.c.) was about equipotent but the inhibition lasted longer. The effects of both etorphine and methadone were completely antagonized by naloxone (1 mg/kg s.c.) and to a lesser extent by diprenorphine (10 μg/kg s.c.). Yohimbine did not suppress the inhibitory effect of etorphine on protein output but showed some antagonism against the effects of etorphine on water and bicarbonate output. In anaesthetized rats etorphine (3 μg/kg) inhibited the pancreatic secretion stimulated by 2-deoxy glucose, a centrally acting vagal stimulatory agent, by 50–60% for volume and bicarbonate output and totally for protein output. The same dose of etorphine did not inhibit the pancreatic secretion evoked by vagal electrical stimulation, a peripheral stimulus. Methadone (5 mg/kg) inhibited the pancreatic secretion stimulated by 2-deoxy glucose to the same extent, but for a longer time than etorphine, and at the same dose did not suppress the pancreatic response to vagal electrical stimulation. The inhibitory effects of etorphine and methadone in anaesthetized rats were completely suppressed by naloxone (1 mg/kg s.c.) and only reduced by diprenorphine (10 μg/kg s.c.). These results suggest that etorphine, like methadone, inhibits exocrine pancreatic secretion in rats by acting mainly on a central mechanism more likely to involve μ than δ opiate receptors

Stimulating effect of duodenal alkalinization on pancreatic exocrine secretion in rats.

Intraduodenal instillations of 1.0 M NaHCO3, 0.1 M Na2CO3, and 0.1 M NaOH in anesthetized rats stimulated significantly the pancreatic exocrine secretion showing 3.8-, 7.1-, and 19.0-fold increase of the pancreatic juice flow, respectively. Protein concentration and amylase activity in pancreatic juice increased after injecting NaOH, but decreased after injecting Na2CO3.

Influence of adrenaline, glucagon, hydrocortisone, thyroxine, or insulin administration on pancreatic exocrine secretion in rats.

Pancreatic exocrine response induced by CCK-PZ (0.2 U/100 g body weight)and amylase content were studied in rats which had been treated with adrenaline, glucagon, hydrocortisone, thyroxine and insulin for 7 days. After insulin or thyroxine treatment, the basal level of pancreatic juice flow and protein output was higher, and the CCK-PZ induced responses were 3-fold larger than those of the corresponding controls. CCK-PZ induced juice flow in hydrocortisone treatment was depressed, but the protein output was not. The ratio of amylase to protein in pancreatic juice and pancreas decreased after adrenaline, glucagon, or thyroxine treatment, but not after insulin or hydrocortisone treatment. Changes in plasma concentration of glucose, free fatty acid and insulin were not correlated directly with a decrease in the amylase content after adrenaline, glucagon or thyroxine treatment. The results indicate the possibility that adrenaline, glucagon, thyroxine and insulin can modify the synthesis and/or release of pancreatic amylase.