Effects of adenosine, adenosine triphosphate and structural analogues on glucagon secretion from the perfused pancreas of rat <i>in vitro</i>

Chapal, J; Loubatières-Mariani, Marie-Madeleine; Roye, M; Zerbib, A.

doi:10.1111/j.1476-5381.1984.tb16533.x

Cited by 22 publications

(15 citation statements)

References 21 publications

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“…The activation of these receptors induced a transient increase of glucagon secretion. We have also shown that ATP was effective after hydrolysis to adenosine (Chapal et al, 1984). It is now generally accepted that there are two subtypes of extracellular receptors involved in the action of adenosine.…”

Section: Introductionmentioning

confidence: 72%

Evidence for an A₂‐subtype adenosine receptor on pancreatic glucagon secreting cells

Chapal

Petit

et al. 1985

British J Pharmacology

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1 The effects of a 5'-substituted analogue of adenosine, 5'-N-ethylcarboxamidoadenosine (NECA) have been studied on glucagon secretion in vitro, using the isolated pancreas of the rat perfused in the presence of glucose (2.8 mM). 2 NECA provoked a peak of glucagon secretion, the kinetics of which were comparable to those previously obtained with adenosine. The effect was concentration-dependent and appeared at nanomolar concentrations. The EC50 was approximately 4 x 10-8 M. 3 A comparison of relative potency between adenosine and NECA showed that NECA was about 800 fold more potent than adenosine in inducing glucagon secretion.4 Theophylline (50 pM) considerably decreased the peak of glucagon secretion induced by 1.65 gM NECA and totally suppressed the effect of 16.5 nM NECA. These results indicate the involvement of an adenosine receptor. 5 These and other previous results (low stereoselectivity of N6-phenylisopropyladenosine) provide evidence for an adenosine receptor of the A2-subtype being involved in glucagon secretion.

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Section: Introductionmentioning

confidence: 72%

Evidence for an A₂‐subtype adenosine receptor on pancreatic glucagon secreting cells

Chapal

Petit

et al. 1985

British J Pharmacology

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“…Consequently, not only ATP and ADP but also their more stable /a/p-methylene analogues induced mobilization, whereas AMP, adenosine and P/y-methylene ATP were without obvious effects. Measurements of the release ofinsulin and glucagon from the perfused rat pancreas have provided evidence for the existence of P,-purinoceptors in the a2-cells and P2-receptors in the P-cells (Loubatieres-Mariani et al, 1979;Chapal & Loubatieres-Mariani, 1981;Chapal et al, 1984). It should be emphasized that pancreatic islets from obh ob-mice are practically devoid of the glucagonproducing a2-cells (Hellman, 1965).…”

Section: Discussionmentioning

confidence: 99%

External ATP mimics carbachol in initiating calcium mobilization from pancreatic β‐cells conditioned by previous exposure to glucose

Gylfe

Hellman

1987

British J Pharmacology

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1 Exposure to ATP (2-200 pM) resulted in a prominent peak of 45Ca efflux, when P-cell-rich pancreatic islets from ob/ob-mice were perifused with a Ca2+-deficient medium. ADP and the stable /x/p-methylene analogues of ATP and ADP also had stimulatory effects. 2 The nucleotide initiation of "5Ca efflux mimicked that obtained with carbachol both in requiring previous exposure to glucose and in being more pronounced after replacing extracellular Na+ by K+. 3 It was possible to induce repeated peaks of stimulated 45Ca efflux, when the exposure to ATP was interrupted with intervals of perifusion with glucose-containing media. 4 The observations are consistent with the existence of P2-purinoceptors in islets, suggesting that these receptors mediate a similar mobilization of calcium as noted when activating polyphosphoinositide breakdown with carbachol. In view of the high contents of ATP and ADP in the 13-cell secretory granules, activation of P2-purinoceptors should be considered as a possible mechanism for amplification of the initial insulin secretory response.

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“…NECA, induced dose-dependent glucagon release from α cells, presumably via A 2 receptors [39,41,42]. These actions were eliminated by aminophylline and theophylline.…”

Section: Endocrine Pancreas β Cellsmentioning

confidence: 91%

Purinergic receptors in the endocrine and exocrine pancreas

Novak

2007

Purinergic Signalling

115

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The pancreas is a complex gland performing both endocrine and exocrine functions. In recent years there has been increasing evidence that both endocrine and exocrine cells possess purinergic receptors, which influence processes such as insulin secretion and epithelial ion transport. Most commonly, these processes have been viewed separately. In β cells, stimulation of P2Y 1 receptors amplifies secretion of insulin in the presence of glucose. Nucleotides released from secretory granules could also contribute to autocrine/paracrine regulation in pancreatic islets. In addition to P2Y 1 receptors, there is also evidence for other P2 and adenosine receptors in β cells (P2Y 2 , P2Y 4 , P2Y 6 , P2X subtypes and A 1 receptors) and in glucagon-secreting α cells (P2X 7 , A 2 receptors). In the exocrine pancreas, acini release ATP and ATP-hydrolysing and ATP-generating enzymes. P2 receptors are prominent in pancreatic ducts, and several studies indicate that P2Y 2 , P2Y 4 , P2Y 11 , P2X 4 and P2X 7 receptors could regulate secretion, primarily by affecting Cl − and K + channels and intracellular Ca 2+ signalling. In order to understand the physiology of the whole organ, it is necessary to consider the full complement of purinergic receptors on different cells as well as the structural and functional relation between various cells within the whole organ. In addition to the possible physiological function of purinergic receptors, this review analyses whether the receptors could be potential therapeutic targets for drug design aimed at treatment of pancreatic diseases.

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Effects of adenosine, adenosine triphosphate and structural analogues on glucagon secretion from the perfused pancreas of rat in vitro

Cited by 22 publications

References 21 publications

Evidence for an A₂‐subtype adenosine receptor on pancreatic glucagon secreting cells

Evidence for an A₂‐subtype adenosine receptor on pancreatic glucagon secreting cells

External ATP mimics carbachol in initiating calcium mobilization from pancreatic β‐cells conditioned by previous exposure to glucose

Purinergic receptors in the endocrine and exocrine pancreas

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Effects of adenosine, adenosine triphosphate and structural analogues on glucagon secretion from the perfused pancreas of rat in vitro

Cited by 22 publications

References 21 publications

Evidence for an A2‐subtype adenosine receptor on pancreatic glucagon secreting cells

Evidence for an A2‐subtype adenosine receptor on pancreatic glucagon secreting cells

External ATP mimics carbachol in initiating calcium mobilization from pancreatic β‐cells conditioned by previous exposure to glucose

Purinergic receptors in the endocrine and exocrine pancreas

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Evidence for an A₂‐subtype adenosine receptor on pancreatic glucagon secreting cells

Evidence for an A₂‐subtype adenosine receptor on pancreatic glucagon secreting cells