Inhibition of Exocrine Pancreatic Secretion by Somatostatin in Dogs

Susini, C.; Estève, Jean-Pierre; Bommelaer, Gilles; Vaysse, N.; Ribet, A

doi:10.1159/000198224

Cited by 30 publications

(8 citation statements)

References 17 publications

(26 reference statements)

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“…Somatostatin dose-dependently inhibits exocrine secretion of various gastrointestinal organs (such as secre tion of gastric acid and pepsinogen, pancreatic secretion, bile flow, and ductular hepatic secretion) [40,61,62], and neuroendocrine secretion (such as secretion of gastrin, CCK, secretin, VIP (vasoactive intestinal polypeptide), G1P (gastric inhibitory polypeptide), motilin, acetylcho line, insulin, glucagon, and pancreatic polypeptide) [33, 39, 44, 46, 60, 63. 64], There is general agreement that exogenous somatosta tin dose-dependently inhibits interdigestive pancreatic enzyme secretion in the experimental animal [47,58,65] and in humans [66,67], Studies on its effects on interdi gestive water and bicarbonate secretion show, however, conflicting results [42,57], Somatostatin markedly inhib ited pancreatic enzyme secretion in animals [47,58,65,68,69] and humans [52,53,57,66,70] stimulated by var ious peptides and neural mechanisms [47,65,68].…”

Section: Biologic Functions Of Somatostatin and Octreotidementioning

confidence: 99%

“…Almost all investigators agree that somatostatin mark edly inhibits pancreatic enzyme secretion in intact ani mals [47,58,65,68,69] and humans [52,53,57,66,70] stimulated by various peptides.…”

Section: Effects Of Somatostatin and Its Analogues On Pancreatic Secrmentioning

confidence: 99%

“…Somatostatin, in particular, inhibited secretin-stimu lated pancreatic secretion in dogs [54,58] and humans [50] but not in pigs [82] and rats [47,83]. CCK-stimulated pancreatic secretion was inhibited by somatostatin in most species including humans [83,84], The studies which evaluated the effect of somatostatin on CCK-stim ulated secretion in dogs report controversial results: one study showed an inhibitory effect [85] whereas another study failed to show such inhibition [58].…”

Section: Effects Of Somatostatin and Its Analogues On Pancreatic Secrmentioning

confidence: 99%

“…The lack of somatostatin to inhibit secretin-stimulated bicarbonate and fluid secretion increase in previous stud ies might be due to supraphysiologic doses of secretin used in these experiments [73], Thus, the effect of somatostatin and octreotide on pan creatic bicarbonate and fluid secretin remains somewhat controversial. Some studies did report an inhibitory effect of somatostatin on secretin-stimulated pancreatic bicar bonate and fluid secretion [50,54,58,73,74] whereas most others did not [14,28,45,51,54,85,88]. Somatosta tin inhibited amylase secretion [89] but failed to inhibit bicarbonate secretion in response to exogenous VIP [90], Most studies agree that somatostatin also inhibits neu ral stimulation of pancreatic secretion.…”

Section: Effects Of Somatostatin and Its Analogues On Pancreatic Secrmentioning

confidence: 99%

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Inhibition of Exocrine Pancreatic Secretion by Somatostatin and Its Analogues

Heintges¹,

Lüthen²,

Niederau³

1994

Digestion

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The stimulation of exocrine pancreatic secretion has extensively been studied in the past. On the other hand, little is known about the factors and mechanisms which regulate inhibition of exocrine pancreatic secretion. This review, therefore, focuses on somatostatin as one candidate of several peptides which may physiologically mediate inhibition of pancreatic secretion and on its possible mode of action. Somatostatin probably inhibits pancreatic exocrine secretion by a variety of mechanisms which depend on the species and the type of secretion studied (postprandial vs. interdigestive secretion, protein vs. bicarbonate secretion): Somatostatin may act via inhibition of the release of circulating hormones such as cholecystokinin (CCK) and secretin or via intra-pancreatic inhibition of the release or action of CCK. Somatostatin may inhibit acetylcholine release from nerve terminals which express specific somatostatin receptors or directly affect the secretory response of the acinar cells via specific somatostatin receptors by a reduction of intracellular cAMP. Somatostatin may also indirectly alter the pancreatic response to a meal by its extra-pancreatic effects, e.g. inhibition of gastric secretion, gastric emptying, gallbladder emptying and gastrointestinal motility.

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Section: Biologic Functions Of Somatostatin and Octreotidementioning

confidence: 99%

Section: Effects Of Somatostatin and Its Analogues On Pancreatic Secrmentioning

confidence: 99%

Section: Effects Of Somatostatin and Its Analogues On Pancreatic Secrmentioning

confidence: 99%

Section: Effects Of Somatostatin and Its Analogues On Pancreatic Secrmentioning

confidence: 99%

See 2 more Smart Citations

Inhibition of Exocrine Pancreatic Secretion by Somatostatin and Its Analogues

Heintges¹,

Lüthen²,

Niederau³

1994

Digestion

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“…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].…”

mentioning

confidence: 99%

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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Trophic Effects of Gut Peptides

Johnson

1989

Comprehensive Physiology

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Inhibition of Exocrine Pancreatic Secretion by Somatostatin in Dogs

Cited by 30 publications

References 17 publications

Inhibition of Exocrine Pancreatic Secretion by Somatostatin and Its Analogues

Inhibition of Exocrine Pancreatic Secretion by Somatostatin and Its Analogues

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

Trophic Effects of Gut Peptides

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