Characterization of the three different states of the cholecystokinin (CCK) receptor in pancreatic acini

Talkad, Venugopal D.; Patto, Renato J.; Metz, David C.; Turner, R; Fortune, Kirk P.; Bhat, Sanjay T.; Gardner, Jerry D.

doi:10.1016/0167-4889(94)90118-x

Cited by 24 publications

(12 citation statements)

References 16 publications

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“…The decrease in affinity of CCK-8 for the low-affinity state of the receptor illustrated in Fig. 4 and Table 2 is not sufficient to alter the potency with which CCK-8 stimulates amylase secretion, because occupation of only a small fraction of the low-affinity receptors produces maximal stimulation of secretion (10).…”

mentioning

confidence: 99%

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Modulation of cholecystokinin activity by albumin.

Huang¹,

Talkad²,

Fortune³

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

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mentioning

confidence: 99%

“…The data in Fig. 4 Left were analyzed using the LIGAND program (20 (8)(9)(10). As illustrated in Fig.…”

mentioning

confidence: 99%

Modulation of cholecystokinin activity by albumin.

Huang¹,

Talkad²,

Fortune³

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

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“…According to this model, the function of the high affinity state is unknown, low affinity binding evokes [Ca 2+ ] i oscillations and stimulation of amylase release, and the very low affinity binding is related to sustained elevation of [Ca 2+ ] i and in accordance with a previous proposal (Sjödin et al 1991) supramaximal inhibition of secretion (Talkad et al 1994b). The present results from the guinea pig appear consistent with the model of Talkad et al (1994b). It is tempting to speculate that a similar model is valid for cholinergic stimulation with the sustained elevation related to interaction with a so far unidentified very low affinity state of the receptor.…”

Section: Discussionmentioning

confidence: 77%

“…Studies of rat pancreatic acinar cells have indicated three different states for CCK-8 with K D values of 1 nM (high affinity), 30 nM (low affinity) and 13 µM (very low affinity; Talkad et al 1994b). According to this model, the function of the high affinity state is unknown, low affinity binding evokes [Ca 2+ ] i oscillations and stimulation of amylase release, and the very low affinity binding is related to sustained elevation of [Ca 2+ ] i and in accordance with a previous proposal (Sjödin et al 1991) supramaximal inhibition of secretion (Talkad et al 1994b). The present results from the guinea pig appear consistent with the model of Talkad et al (1994b).…”

Section: Discussionmentioning

confidence: 99%

Cholecystokinin-JMV-180 and pilocarpine are potent inhibitors of cholecystokinin and carbachol actions on guinea pig pancreatic acinar cells

Sjödin

Viitanen

Gylfe

1997

Naunyn-Schmiedeberg's Arch Pharmacol

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The release of amylase and the elevation of cytoplasmic Ca2+ concentration ([Ca2+]i) in response to cholecystokinin-octapeptide (CCK-8), the cholecystokinin analogue JMV-180, the stable choline ester carbamylcholine (carbachol) and the muscarinic agonist pilocarpine were studied in guinea-pig pancreatic acinar cells. The maximal amylase and [Ca2+]i responses to JMV-180 and pilocarpine were 12-15% of the corresponding responses to CCK-8 and carbachol. The amylase and [Ca2+]i responses to maximal concentrations of CCK-8 and carbachol were inhibited in concentration-dependent manners by JMV-180 and pilocarpine, respectively. In individual acinar cells, JMV-180 and pilocarpine like low concentrations of CCK-8 and carbachol caused oscillations of [Ca2+]i. The sustained [Ca2+]i responses to maximal concentrations of CCK-8 and carbachol were transformed into oscillatory responses during simultaneous exposure to JMV-180 and pilocarpine, respectively. Maximal concentrations of JMV-180 and pilocarpine did not cause homologous or heterologous desensitization of the [Ca2+]i responses but inhibited desensitization evoked by maximal concentrations of CCK-8 or carbachol. JMV-180 and pilocarpine acted as weak, partial agonists exhibiting effective inhibition of the acinar cell responses to full agonists. The effects appeared to be best explained by interactions with two forms of the respective receptor with JMV-180 and pilocarpine acting as partial agonists for one state of the receptor and as antagonist for the second state.

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“…The pancreatic CCK A and CCK B receptors in rodents can exist in different states with high or low binding affinity towards CCK [21, 22]. The low affinity CCK A receptor state leads to translocation and activation of PKCδ downstream of Src family kinases [23].…”

Section: Pkc In Normal Pancreatic Functionsmentioning

confidence: 99%

Protein kinase C isoforms in the normal pancreas and in pancreatic disease

Fleming

Störz

2017

Cellular Signalling

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Protein Kinase C isoforms have been implicated in regulating multiple processes within the healthy pancreas. Moreover, their dysregulation contributes to all aspects of pancreatic disease. In this review, with a focus on acinar, ductal, and islet cells, we highlight the roles and contributions of the different PKC isoforms to normal pancreas function. We also discuss the contribution of PKC enzymes to pancreatic diseases, including insulin resistance and diabetes mellitus, as well as pancreatitis and the development and progression of pancreatic cancer.

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Characterization of the three different states of the cholecystokinin (CCK) receptor in pancreatic acini

Cited by 24 publications

References 16 publications

Modulation of cholecystokinin activity by albumin.

Modulation of cholecystokinin activity by albumin.

Cholecystokinin-JMV-180 and pilocarpine are potent inhibitors of cholecystokinin and carbachol actions on guinea pig pancreatic acinar cells

Protein kinase C isoforms in the normal pancreas and in pancreatic disease

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