Mechanism of action of magnesium on acetylcholine‐evoked secretory responses in isolated rat pancreas

Francis, LP; Lennard, Roger; Singh, Jaipaul

doi:10.1113/expphysiol.1990.sp003445

Cited by 35 publications

(19 citation statements)

References 22 publications

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“…In (Lennard & Singh, 1992), we demonstrated that basal [Mg2+]I changes during perturbation of extracelluar Mg2+. Taken together, these results corroborate previous findings using acetylcholine (Francis et al 1990) that an alteration in cellular Mg2+ can influence secretagogue-evoked exocrine secretion in the pancreas. Vicinal diones are reagents which are recognized to react with and modify arginine residues in proteins (Lundblad & Noyes, 1984).…”

supporting

confidence: 82%

Proceedings of the Physiological Society, 17‐18 December 1992, Queen Mary and Westfield College Meeting: Communications

1993

The Journal of Physiology

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supporting

confidence: 82%

Proceedings of the Physiological Society, 17‐18 December 1992, Queen Mary and Westfield College Meeting: Communications

1993

The Journal of Physiology

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“…The pancreas of either normal or diabetic female rats was dissociated into acinar cells with collagenase in two stages totalling 75 min by established methods (Francis et al 1990b;Francis & Singh, 1990). Pancreatic acinar cells were loaded with 2 ìÒ fura_2-acetomethylester (AM) by methods described previously (Francis et al 1990a).…”

Section: Measurement Of [Ca¥]é In Pancreatic Acini and Acinar Cellsmentioning

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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“…Concerning the precise mechanism for this action of catecholamines on Mg 2+ movements, an increase in the affinity of the Mg 2+ transporter for intracellular Mg 2+ through cAMPactivated phosphorylation has been postulated (86). (43,44,102,152,153). In these experiments, the individual enzyme and total protein secretion were determined by on-line automated methods (152,(154)(155)(156)) based on either fluorimetric or colorimetric measurements.…”

Section: Other Tissuesmentioning

confidence: 99%

“…(43,44,102,152,153). In these experiments, the individual enzyme and total protein secretion were determined by on-line automated methods (152,(154)(155)(156)) based on either fluorimetric or colorimetric measurements. The same effect of high [Mg 2+ ] o is observed in isolated intact pancreas with respect to the pancreatic flow rate and total protein output (44).…”

Section: Other Tissuesmentioning

confidence: 99%

“…IP 3 , in turn, mobilizes Ca 2+ from endoplasmic reticulum (ER) stores (157), the Ca 2+ -signaling events finally leading to exocytosis and enzyme secretion. Maximal agonist concentrations induce a large and dual Ca 2+ response (40,41,44,152) in which the initial increase has been attributed to Ca 2+ released from intracellular stores and the later sustained phase due to influx of Ca 2+ across the basolateral membrane (158). Submaximal agonist concentrations evoke oscillating cytoplasmic Ca 2+ spikes (46,102).…”

Section: Relationship Between Calcium and Magnesium Signaling In The mentioning

confidence: 99%

See 1 more Smart Citation

Intracellular magnesium: transport and regulation in epithelial secretory cells

Yago

Mañas²,

Singh³

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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Mechanism of action of magnesium on acetylcholine‐evoked secretory responses in isolated rat pancreas

Cited by 35 publications

References 22 publications

Proceedings of the Physiological Society, 17‐18 December 1992, Queen Mary and Westfield College Meeting: Communications

Proceedings of the Physiological Society, 17‐18 December 1992, Queen Mary and Westfield College Meeting: Communications

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

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