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Cadmium inhibits stimulated amylase secretion from isolated pancreatic lobules of the guinea-pig
No full textThe effect of cadmium chloride on pancreatic exocrine secretion 'in vitro' was examined using guinea-pig isolated lobules, Cadmium (10(-3) M) stimulated amylase release when added alone to the incubation medium and the increase of amylase was unaffected by atropine. Cadmium (10(-4) M) did not significantly modify the basal amylase release. Depolarization of pancreatic nerves with potassium stimulated amylase secretion; the stimulant effect of KCl was completely inhibited by atropine. Cadmium (10(-4) M) inhibited, but did not abolish, the stimulant effect of KCl, indicating a direct effect of the metal on the acinar cell. Cadmium (10(-4) M) also inhibited the amylase release evoked by the secretagogues carbachol and caerulein, which are known to act directly on the acinar cell. Taken together with previous data reporting a large increase of pancreatic cadmium concentration following cadmium ingestion, the strong inhibition of pancreatic secretion observed in our experiments suggests that the exocrine pancreas may be regarded as a possible target organ of cadmium toxicity. (C) 2001 Academic Press
The effect of the selective NK3 receptor agonists, PGKII and senktide, on in vitro exocrine pancreatic secretion in the guinea pig.
No full textRegulation of pancreatic secretion in vitro by nociceptin/orphanin FQ and opioid receptors: A comparative study
No full textThe effects of nociceptin/orphanin FQ (N/OFQ) on gastrointestinal functions resemble those of classic analgesic opioid agonists. In this study, we compared changes in amylase release from guinea pig isolated pancreatic acini and lobules induced by the N/OFQ analogue [Arg(14) Lys(15)]N/OFQ and by the delta-receptor opioid agonist deltorphin. Carbachol strongly stimulated amylase release from isolated acini. Both peptides left baseline and carbachol-stimulated amylase secretion from pancreatic acini unchanged. Co-incubation of KCI-stimulated lobules with [Arg(14),Lys(15)]N/OFQ or deltorphin inhibited KCI-induced amylase release in a concentration-dependent manner. Although maximal inhibition of amylase release by [Arg(14),Lys(15)]N/OFQ and deltorphin had similar amplitude, [Arg(14),Lys(15)]N/OFQ was 100-fold more potent than deltorphin on a molar basis. The selective NOP-receptor antagonist [Nphe(1),Arg(14),Lys(15)]N/OFQ-NH2 (UFP-101) antagonized [Arg(14),Lys(15)]N/OFQ-induced inhibition but left deltorphin-induced inhibition unchanged. The selective delta opiate receptor antagonist naltrindole had no effect on [Arg(14),Lys(15)]N/OFQ inhibition but partly prevented the inhibition by deltorphin. [Arg(14)Lys(15)]N/OFQ and deltorphin combined had no influence on each other. These findings show that [Arg(14),Lys(15)]N/OFQ inhibits pancreatic enzyme secretion by suppressing cholinergic transmission in intralobular nerve fibers, as previously reported for opioid agents. They suggest that [Arg(14),Lys(15)]N/OFQ inhibition of amylase release is mediated through the NOP receptor and not through the delta opioid receptor. The N/OFQ-NOP receptor system, like the delta opioid system, plays an inhibitory role in regulating exocrine pancreatic secretion. (c) 2006 Elsevier Ltd. All rights reserved
The cannabinoid win 55,212 inhibits pancreatic amylase secretion via cholinergic suppression
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The effect of orphanin FQ on some in vivo and in vitro gastrointestinal functions.
No full textPharmacol. Res. (43, p. 115
Selective tachykinin NK3-receptor agonists stimulate in vitro exocrine pancreatic secretion in the guinea pig
No full textThe tachykinins, including substance P, neurokinin A and neurokinin B, are a mammalian peptide family that have documented motor, sensory and circulatory neurotransmitter functions in the gut. Little is known about their action on the exocrine pancreas. In this study we investigated the effects of PG-KII, a natural NK3-tachykinin receptor agonist, and senktide, a synthetic NK3-tachykinin receptor agonist, on amylase release from isolated pancreatic lobules of the guinea pig in comparison with the secretagogues carbachol, caerulein and substance P and the depolarizing agent KCl. When added to incubation flasks at various concentrations (from 10(-10) to 10(-6) M), PG-KII and senkfide both caused a dose-dependent increase in amylase release from pancreatic lobules. PG-KII and senktide elicited a lower maximal response (7.5 +/- 0.8 and 8.1 +/- 0.6% of the total lobular amylase content) than carbachol (34.4 +/- 3.9%), caerulein (26.5 +/- 2.8%) and KCl (22.5 +/- 3.8%). Whereas atropine left PG-KII and senktide-stimulated secretion unaffected, the non peptide NK3 receptor antagonist SR 142801 significantly reduced the stimulant effect of PG-KII and senktide. PG-KII (10(-7) M) also slightly though significantly increased the response to lower concentrations of caerulein (10(-11) and 10(-10) M) and carbachol (10(-7) and 10(-6) M). These findings show that PG-KII and senkfide are weak stimulants of exocrine pancreatic secretion that act directly on the acinar cells through NK3 receptors, without cholinergic involvement. We suggest also that the tachykininergic NK3 receptor system cooperates with the other known secretagogues in the control of pancreatic exocrine secretion. (C) 2002 Elsevier Science Inc. All rights reserved
A comparative study of the effect of (Arg 14, Lys 15)N/OFQ and deltorphin on exocrine pancreatic secretion in vitro.
No full textEthanol combined with cocaine inhibits amylase release in guinea pig pancreatic lobules
No full textConcurrent ingestion of alcohol and cocaine is a common occurrence in cocaine-dependent individuals. Cocaethylene is a pharmacologically active metabolite of cocaine that is formed in the liver in the presence of ethanol. The effects of ethanol combined with cocaine on the exocrine pancreas are not known. We studied the effect of ethanol and cocaine, alone or in combination, and cocaethylene on amylase release from isolated lobules of the guinea pig pancreas. Incubation of lobules with ethanol plus cocaine produced a more evident reduction of amylase release than each drug alone. An even larger reduction was observed with cocaethylene. HPLC analysis of incubation medium showed that no cocaethylene was formed in vitro in the presence of ethanol anti cocaine. It is concluded that cocaethylene could strongly contribute to inhibition of exocrine pancreatic secretion in individuals who coadminister alcohol with cocaine. (C) 2001 Academic Press
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