Interaction between secretin and nerve‐mediated amylase secretion in the isolated exocrine rat pancreas

Wisdom, Denham M.; Camello, PJ; Salido, Ginés M.; Singh, Jaipaul

doi:10.1113/expphysiol.1994.sp003813

Cited by 14 publications

(13 citation statements)

References 20 publications

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“…For example the phorbol esters can potentiate the secretory actions of ACh and noradrenaline (NA) (Singh, 1985a;Francis & Singh, 1990) and attenuate enzyme secretion evoked by CCK-8 (Ansah et al 1986;Francis et al 1990a). Similarly, secretin can attenuate the secretagogue effect of CCK-8 and activation of intrinsic nerves in the rat pancreas (Singh et al 1992;Wisdom et al 1994).…”

Section: Introductionmentioning

confidence: 99%

Interaction of Islet Hormones with Cholecystokinin Octapeptide‐Evoked Secretory Responses in the Isolated Pancreas of Normal and Diabetic Rats

Singh

Adeghate

Salido

et al. 1999

Experimental Physiology

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summaryThis study investigates the effects of the islet hormones, insulin (Ins), glucagon (Glu) and somatostatin (Som) with cholecystokinin octapeptide (CCK-8) on amylase secretion and intracellular free calcium concentration [Ca¥]é and their pattern of distribution in the isolated pancreas of normal and diabetic rats. Ins and Glu evoked small increases in amylase output from pancreatic segments compared with a much enhanced effect of CCK-8. In contrast, Som induced a biphasic response comprising an initial decrease followed by a secondary increase and this biphasic response may be dependent upon the concentration. Combining the islet hormones with CCK-8 resulted in marked potentiation in amylase output compared with either CCK-8 alone or the individual hormone. Genistein and tyrphostin A25, the tyrosine kinase inhibitors, evoked a small decrease in amylase output from pancreatic segments. They had no effect on the CCK-8-evoked secretory response but markedly inhibited the potentiation of the islet hormones with CCK-8. In pancreatic acini and acinar cells Ins, Glu and Som individually evoked small increases in amylase output compared with a much larger response with CCK-8. When the islet hormones were combined with CCK-8 there was no potentiation of amylase output. Similarly, when rats were rendered diabetic by prior treatment with streptozotocin Ins, Glu and Som failed to potentiate the secretory response of CCK-8. In fura_2-loaded pancreatic acinar cells Ins or Glu evoked small increases in [Ca¥]é compared with a much larger elevation with CCK-8. Ins, Glu and Som each enhanced the CCK-8-evoked [Ca¥]é. Genistein elicited a decrease in [Ca¥]é both in the absence and presence of the islet hormones. It also decreased the elevation in [Ca¥]é resulting from the combined presence of CCK-8 with either Ins or Glu but it had no effect on CCK-8 in combination with Som. In pancreatic acinar cells from diabetic rat Ins, Glu and Som had no detectable effect on CCK-8-evoked elevation in [Ca¥]é compared with the response obtained with CCK-8 alone. CCK-8-immunopositive cells were distributed around the walls of blood vessels, numerous Inspositive cells in the central and peripheral parts of the islets of Langerhans, Glu-immunoreactive cells in the periphery of islets and Som-positive cells in the outer part of the islets. During diabetes, the number of CCK-immunopositive cells remained unchanged whereas the number of Inspositive cells decreased coupled with an increase in the number of Glu-positive cells. The results indicate that both tyrosine kinase and cellular Ca¥ seem to be the intracellular mediators involved with the enhanced secretory responses obtained with a combination of the islet hormones with CCK-8. Moreover, the presence of viable pancreatic islets of Langerhans seems to be associated with the potentiation of the islet hormones with CCK-8.

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Section: Introductionmentioning

confidence: 99%

Interaction of Islet Hormones with Cholecystokinin Octapeptide‐Evoked Secretory Responses in the Isolated Pancreas of Normal and Diabetic Rats

Singh

Adeghate

Salido

et al. 1999

Experimental Physiology

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“…A similar Na + -dependency on Mg 2+ transport has been observed in single mouse pancreatic acinar cells (102). The existence of a Na + /Ca 2+ exchanger has been demonstrated in rat and mouse pancreatic acinar cells (139) and, in fact, we were able to show that the application of a Na (40)(41)(42)(43)45). …”

Section: Exocrine Pancreasmentioning

confidence: 54%

“…Loading times are short and no detectable compartmentalization is evident. From our studies using dual wavelength fluorimetry with Magfura-2, it would appear that resting [Mg 2+ ] i in both rat and mouse pancreatic acinar cells is about 0.8 mM (41)(42)(43)(44)(45)(46), which is very similar to the value found by other authors with the same technique in pancreatic beta cells (35). Accordingly, using this approach, [Mg 2+ ] i between 0.9 and 1 mM have been reported in heart tissue as measured with Mg 2+ -selective microelectrodes (47)(48)(49) as well as in skeletal muscle as determined by 31 P NMRs (50).…”

Section: +mentioning

confidence: 88%

“…The affinity of Magfura-2 for Ca 2+ is not very different from that for Mg 2+ (29) and several authors have indicated the existence of a clear interference from this source (54,55 (40,41) or single cell studies (46,51). In addition, different approaches can be undertaken, including perfusion of the tissue (28,46) or the employment of static-volume cuvettes (42,43).…”

Section: +mentioning

confidence: 99%

“…Our experiments using either a suspension of rat pancreatic acinar cells or single mouse acinar cells loaded with Magfura-2 AM showed that acetylcholine (ACh), carbamylcholine cholecystokinin-octapeptide (CCK-8), thapsigargin and ionomycin, all well known Ca 2+ -mobilising agents, induce marked changes in [Mg 2+ ] i , consisting of a sharp and transient rise, immediately followed by a gradual decline to reach a steady-state significantly lower than the resting value, which is maintained throughout the experiment (40)(41)(42)(43)45,46,102,127,130). The decrease revealed a dosedependency with secretagogues, and atropine blocked the ACh-evoked response.…”

Section: Exocrine Pancreasmentioning

confidence: 99%

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Intracellular magnesium transport and regulation in epithelial secretory cells

Singh¹

2000

Front Biosci

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ABSTRACT] i from magfura-2-loaded acini and acinar cells and Mg 2+ content in effluent samples from perfused pancreatic segments, respectively, confirm that secretagogues such as acetylcholine (ACh) and cholecystokinin-octapeptide (CCK-8) can evoke marked and significant extrusion of Mg 2+ which is closely associated with the mobilization of intracellular calcium. These effects may be modulated by different mediators including cAMP, Protein Kinase C and nitric oxide/cGMP. This reduction in [Mg 2+ ] i seems to be a prerequisite for optimal generation and maintenance of the calcium signal and subsequently, the secretion of enzymes, since an increase in extracellular Mg

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Duck Pancreatic Acinar Cell as a Unique Model for Independent Cholinergic Stimulation–Secretion Coupling

2009

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This paper investigated the role of acetylcholine (ACh) in physiological regulation of amylase secretion in avian exocrine pancreas. In the isolated duck pancreatic acini, ACh dose dependently stimulated amylase secretion, with a maximal effective concentration at 10 muM. The cAMP-mobilizing compounds forskolin, vasoactive intestinal peptide (VIP)/pituitary adenylate cyclase activating peptide (PACAP) receptor (VPAC) agonists PACAP-38 and PACAP-27 had no effect on the dose-response curve. ACh dose dependently induced increases in cytosolic Ca(2+) concentration ([Ca(2+)]( c )), with increasing concentrations transforming oscillations into plateau increases. Forskolin (10 muM), PACAP-38 (1 nM), PACAP-27 (1 nM), or VIP (10 nM) alone did not stimulate [Ca(2+)]( c ) increase; neither did they modulate ACh-induced oscillations, nor made ACh low concentration effective. These data indicate that ACh-stimulated zymogen secretion in duck pancreatic acinar cells is not subject to modulation from the cAMP signaling pathway; whereas it has been widely reported in the rodents that ACh-stimulated exocrine pancreatic secretion is significantly enhanced by cAMP-mobilizing agents. This makes the duck exocrine pancreas unique in that cholinergic stimulus-secretion coupling is not subject to cAMP regulation.

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Interaction between secretin and nerve‐mediated amylase secretion in the isolated exocrine rat pancreas

Cited by 14 publications

References 20 publications

Interaction of Islet Hormones with Cholecystokinin Octapeptide‐Evoked Secretory Responses in the Isolated Pancreas of Normal and Diabetic Rats

Interaction of Islet Hormones with Cholecystokinin Octapeptide‐Evoked Secretory Responses in the Isolated Pancreas of Normal and Diabetic Rats

Intracellular magnesium transport and regulation in epithelial secretory cells

Duck Pancreatic Acinar Cell as a Unique Model for Independent Cholinergic Stimulation–Secretion Coupling

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