Bimodal regulation of pancreatic exocrine function in vitro by somatostatin-28

Estève, Jean-Pierre; Vaysse, N.; Susini, Christiane; Kunsch, J. M.; Fourmy, Daniel; Pradayrol, Lucien; Wünsch, Erich; Moröder, Luis; Ribet, A

doi:10.1152/ajpgi.1983.245.2.g208

Cited by 24 publications

(18 citation statements)

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“…Furthermore, a previous study has shown that cyclic AMP-dependent protein phosphorylation initiates the acquisition of Ca 2ϩ -sensitivity by the insensitive Ca 2ϩ activated K ϩ channel in guinea-pig pancreatic acinar cells [29]. A single application of somatostatin has been reported to have no effect on resting cyclic AMP-level [13], but it can inhibit cyclic AMP formation induced by secretin in pancreatic acinar cells [15]. These results coincide with ours.…”

Section: Discussionsupporting

confidence: 90%

“…However, its inhibitory effect of somatostatin on the activity of the channel was not complete, suggesting another pathway, if any, being involved. Somatostatin has been reported to induce a production of cyclic GMP in the pancreatic acinar cells [15], and cyclic GMP-dependent kinase has been reported to regulate Islet Hormones Regulate K ϩ Channel Table 4. The mean؎SEM of open-state probability (p) about the effect of somatostatin on a forskolin-induced opening.…”

Section: Discussionmentioning

confidence: 99%

“…In digestive enzyme secretion, for example, insulin potentiates acetylcholine-induced [8,9] and, cholecytokinin-induced amylase secretion [10]. In vivo, somatostatin inhibits both Ca 2ϩ -induced and cyclic AMP-induced amylase secretion [11][12][13][14], but in vitro, a few consistent effects on secretion have been described [13,15]. As for ionic fluid secretion from pancreatic acini, only one report concerns the effect of insulin on cation channel [16].…”

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confidence: 99%

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A Reciprocal Regulation of Ca2+-Activated K+ Channel by Insulin and Somatostatin in Guinea-Pig Pancreatic Acinar Cells.

Yanagisawa¹,

Suzuki²

2001

JJP

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The pancreatic acini are in close contact with the surrounding islets, having no significant fibrous capsules, and receptors of insulin [1][2][3][4] and somatostatin [5,6] on the pancreatic acinar cell have been reported. Therefore, this might eventually enter into very close interrelation between the exocrine pancreas and the endocrine islet of Langerhans.The secretion of the pancreatic acinar cells has for a long time been thought to be regulated by the islet hormones [7], but few detailed studies indicate hormonal regulation of the acinar cells. In digestive enzyme secretion, for example, insulin potentiates acetylcholine-induced [8,9] and, cholecytokinin-induced amylase secretion [10]. In vivo, somatostatin inhibits both Ca 2ϩ -induced and cyclic AMP-induced amylase secretion [11][12][13][14], but in vitro, a few consistent effects on secretion have been described [13,15]. As for ionic fluid secretion from pancreatic acini, only one report concerns the effect of insulin on cation channel [16].Ca 2ϩ -activated K ϩ channels, which have been suggested to regulate the K ϩ permeability changes in plasma membrane during fluid secretion, have been identified on the basolateral membrane of Cl Ϫ -secreting pancreatic acinar cells in a variety of animal species [17][18][19][20]. It has been suggested that these K ϩ channels are important for Cl Ϫ uptake into cells [21]. Secretagogues evoking an increase in cytoplasmic Ca 2ϩ level activate K ϩ channels causing an increase in the local external K ϩ concentration. Na ϩ , K ϩ , and Cl Key words: insulin, somatostatin, potassium channels, pancreatic juice, cyclic AMP. Abstract:The effects of islet hormones, insulin and somatostatin, on the regulation of the opening of Ca 2ϩ -activated K ϩ channels in the basolateral plasma membrane of primary cultured pancreatic acinar cells of guinea-pig were studied by cell-attached single-channel recording technique. A single application of insulin or somatostatin did not influence the opening of K ϩ channel. The open-state probability (p) of K ϩ channel induced by the application of acetylcholine (ACh) to the bath solution was increased by insulin in the presence of ACh. The enhancement effect of insulin on the increased frequency of the channel opening was not seen when concomitantly applied with protein kinase A inhibitor, Rp-cAMPS triethylamine. Insulin increased the p value of K ϩ channel, which was reversed by an application of somatostatin (Tyr-somatostatin 28). The addition of ACh followed by forskolin or dibutyryl adenosine 3Ј,5Ј-cyclic monophosphate (dbcAMP) to the bath solution evoked an increase in the p value of K ϩ channel. After increasing the channel opening, the addition of somatostatin reduced the p value, but not with dbcAMP. Taken together, the results suggest that insulin and somatostatin reciprocally modify the ACh-induced opening of the Ca 2ϩ -activated K ϩ channel through a cyclic AMP-dependent signaling pathway.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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A Reciprocal Regulation of Ca2+-Activated K+ Channel by Insulin and Somatostatin in Guinea-Pig Pancreatic Acinar Cells.

Yanagisawa¹,

Suzuki²

2001

JJP

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“…However, somatostatin does not inhibit amylase secretion from isolated acini stimulated by caerulein, secretin, vasoactive intestinal polypeptide or carbachol. High doses of somatostatin also stimulate enzyme secretion from isolated acini (Esteve, Vaysse, Susini, Kunsch, Fourmy, Pradayrol, Wunsch, Moroder & Ribet, 1983). Similarly, pancreatic polypeptide, neuropeptide Y and peptide YY inhibit pancreatic exocrine secretion in the intact rat (Louie, Williams & Owyang, 1985).…”

Section: Isolated Vascularly Perfused Pancreasmentioning

confidence: 92%

Calcitonin gene‐related peptide inhibits exocrine secretion from the rat pancreas by a neurally mediated mechanism

Bunnett

Sj²,

Ht³

1991

Experimental Physiology

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SUMMARYThe mechanism by which calcitonin gene-related peptide (CGRP) inhibits exocrine secretion from the rat pancreas was examined in the isolated, vascularly perfused pancreas and in vitro using freshly isolated pancreatic acini. CGRP (10-10-10-7 M) inhibited the volume and protein output from the perfused pancreas, stimulated by a mixture of the cholecystokinin octapeptide CCK8 (10-10 M) and secretin (10-8 M). The inhibition by CGRP was dose related and maximal at 10-8 M (P < 0-05). CGRP (10-8 M) failed to inhibit amylase secretion from isolated pancreatic acini, stimulated by graded concentrations of CCK8 (10-13_10-8 M). This implies an indirect mechanism of inhibition. The mechanism of inhibition was investigated in the isolated, vascularly perfused pancreas using tetrodotoxin, atropine and hexamethonium (all 10-7 M). Tetrodotoxin and atropine but not hexamethonium preveitted the inhibition of volume and protein secretion by CGRP (10-8 M) (P < 0-05). Tetrodotoxin, atropine and hexamethonium were without effect on exocrine secretion stimulated by CCK8 and secretin (controls). These results indicate that CGRP inhibits pancreatic exocrine secretion by an indirect, neurally mediated mechanism involving cholinergic-muscarinic transmission.

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“…It has been shown that somatostatin does not inhibit enzyme secretion in either isolated arterially perfused preparations or acinic cells in vitro (1,6,23,27,40,41), suggesting that the mechanism of inhibition of pancreatic exocrine secretion is indirect. Indeed, there is evidence that somatostatin is likely to exert the inhibitory effect via a central vagal site (19), the sympathetic nerve (22), an intrapancreatic cholinergic pathway (16), or the intrinsic pancreatic peptidergic neurons (26).…”

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confidence: 99%

Microinjection of exogenous somatostatin in the dorsal vagal complex inhibits pancreatic secretion via somatostatin receptor-2 in rats

Liao¹,

Li²,

Lu³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

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Previous studies have suggested that somatostatin inhibits pancreatic secretion at a central vagal site, and the dorsal vagal complex (DVC) is involved in central feedback inhibition of the exocrine pancreas. The aim of this study was to investigate the effect of exogenous somatostatin in the DVC on pancreatic secretion and the somatostatin receptor subtype(s) responsible for the effect. The effects of somatostatin microinjected into the DVC on pancreatic secretion stimulated by cholecystokinin octapeptide (CCK-8) or 2-deoxy-D-glucose (2-DG) were examined in anesthetized rats. To investigate the somatostatin inhibitory action site, a somatostatin receptor antagonist [SRA; cyclo(7-aminoheptanoyl-Phe-D-Trp-Lys-Thr)] was microinjected into the DVC before intravenous infusion of somatostatin and CCK-8/2-DG. The effects of injection of a somatostatin receptor-2 agonist (seglitide) and combined injection of somatostatin and a somatostatin receptor-2 antagonist (CYN 154806) in the DVC on the pancreatic secretion were also investigated. Somatostatin injected into the DVC significantly inhibited pancreatic secretion evoked by CCK-8 or 2-DG in a dose-dependent manner. SRA injected into the DVC completely reversed the inhibitory effect of intravenous administration of somatostatin. Seglitide injected into the DVC also inhibited CCK-8/2-DG-induced pancreatic protein secretion. However, combined injection of somatostatin and CYN 154806 did not affect the CCK-8/2-DG-induced pancreatic secretion. Somatostatin in the DVC inhibits pancreatic secretion via somatostatin receptor-2, and the DVC is the action site of somatostatin for its inhibitory effect. somatostatin; pancreatic exocrine secretion; dorsal vagal complex; dorsal motor nucleus of the vagus nerve; somatostatin receptor antagonist; somatostatin receptor-2 agonist; cholecystokinin octapeptide; 2-deoxy-D-glucose

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Bimodal regulation of pancreatic exocrine function in vitro by somatostatin-28

Cited by 24 publications

References 0 publications

A Reciprocal Regulation of Ca2+-Activated K+ Channel by Insulin and Somatostatin in Guinea-Pig Pancreatic Acinar Cells.

A Reciprocal Regulation of Ca2+-Activated K+ Channel by Insulin and Somatostatin in Guinea-Pig Pancreatic Acinar Cells.

Calcitonin gene‐related peptide inhibits exocrine secretion from the rat pancreas by a neurally mediated mechanism

Microinjection of exogenous somatostatin in the dorsal vagal complex inhibits pancreatic secretion via somatostatin receptor-2 in rats

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