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Adrenaline Stimulates Glucagon Secretion in Pancreatic A-Cells by Increasing the Ca(2+) Current and the Number of Granules Close to the L-Type Ca(2+) Channels

We have monitored electrical activity, voltage-gated Ca(2+) currents, and exocytosis in single rat glucagon-secreting pancreatic A-cells. The A-cells were electrically excitable and generated spontaneous Na(+)- and Ca(2+)-dependent action potentials. Under basal conditions, exocytosis was tightly li...

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Detalles Bibliográficos
Autores principales: Gromada, Jesper, Bokvist, Krister, Ding, Wei-Guang, Barg, Sebastian, Buschard, Karsten, Renström, Erik, Rorsman, Patrik
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1997
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2229364/
https://www.ncbi.nlm.nih.gov/pubmed/9276750
Descripción
Sumario:We have monitored electrical activity, voltage-gated Ca(2+) currents, and exocytosis in single rat glucagon-secreting pancreatic A-cells. The A-cells were electrically excitable and generated spontaneous Na(+)- and Ca(2+)-dependent action potentials. Under basal conditions, exocytosis was tightly linked to Ca(2+) influx through ω-conotoxin-GVIA–sensitive (N-type) Ca(2+) channels. Stimulation of the A-cells with adrenaline (via β-adrenergic receptors) or forskolin produced a greater than fourfold PKA-dependent potentiation of depolarization-evoked exocytosis. This enhancement of exocytosis was due to a 50% enhancement of Ca(2+) influx through L-type Ca(2+) channels, an effect that accounted for <30% of the total stimulatory action. The remaining 70% of the stimulation was attributable to an acceleration of granule mobilization resulting in a fivefold increase in the number of readily releasable granules near the L-type Ca(2+) channels.