α2-Adrenoceptors modulating insulin release from isolated pancreatic islets

@article{Nakaki20042AdrenoceptorsMI,
  title={$\alpha$2-Adrenoceptors modulating insulin release from isolated pancreatic islets},
  author={T. Nakaki and T. Nakadate and R. Kato},
  journal={Naunyn-Schmiedeberg's Archives of Pharmacology},
  year={2004},
  volume={313},
  pages={151-153}
}
SummaryUsing rat isolated pancreatic islets, we investigated the effects of various α-adrenoceptor blocking agents on adrenaline-induced inhibition of glucose-stimulated insulin release. Yohimbine was about 100 times more potent than prazosin in antagonizing the inhibitory effect of adrenaline. At concentrations of 10 μM, phentolamine was about as effective as an antagonist as yohimbine, whereas dihydroergotamine, WB-4101 and phenoxybenzamine were less effective and prazosin produced very… Expand
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TLDR
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TLDR
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TLDR
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TLDR
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SELECTIVE α2 RECEPTOR BLOCKADE FACILITATES THE INSULIN RESPONSE TO ADRENALINE BUT NOT TO GLUCOSE IN MAN
TLDR
The effect of adrenaline on insulin release is mediated by way of inhibitory α2 adrenoceptors in the pancreas, while the release of insulin in response to glucose in a resting subject is independent of the α‐adrenergic system. Expand
Phentolamine, a deceptive tool to investigate sympathetic nervous control of insulin release
TLDR
It is demonstrated that phentolamine is capable of directly stimulating insulin release, and is not an appropriate tool to study possible inhibitory effects of the sympathetic nervous system on insulin release. Expand
α2-Adrenergic stimulation counteracts glucose-induced rise of sodium in pancreatic islets exposed to ouabain
TLDR
It is concluded that activation of α2-adrenoceptors has profound effects on the sodium handling of pancreatic beta-cells exposed to glucose and other stimulators of insulin release. Expand
Adrenergic and nonadrenergic cotransmitters inhibit insulin secretion during sympathetic stimulation in dogs.
TLDR
The results indicate that the inhibitory effects exerted by the sympathetic nervous system on insulin secretion are mediated not only by the classical neurotransmitter norepinephrine acting on alpha 2-adrenoceptors but also by a nonadrenergic cotransmitter that can maintain transmission under conditions of catecholamine deficiency. Expand
B cell adrenoceptors and sulphonylurea-induced insulin release in mouse islets
TLDR
It is concluded that an interaction with B cell adrenoceptors is not involved in the insulinotropic action of sulphonylureas, and blockers of adrenoceptor have, thus, no effect on insulin release in vitro at therapeutic concentrations. Expand
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