Adrenaline Stimulates Glucagon Secretion by Tpc2-Dependent Ca²⁺ Mobilization From Acidic Stores in Pancreatic α-Cells.

ABSTRACT: Adrenaline is a powerful stimulus of glucagon secretion. It acts by activation of β-adrenergic receptors, but the downstream mechanisms have only been partially elucidated. Here, we have examined the effects of adrenaline in mouse and human α-cells by a combination of electrophysiology, imaging of Ca²⁺ and PKA activity, and hormone release measurements. We found that stimulation of glucagon secretion correlated with a PKA- and EPAC2-dependent (inhibited by PKI and ESI-05, respectively) elevation of [Ca²⁺]_i in α-cells, which occurred without stimulation of electrical activity and persisted in the absence of extracellular Ca²⁺ but was sensitive to ryanodine, bafilomycin, and thapsigargin. Adrenaline also increased [Ca²⁺]_i in α

SUBMITTER: Hamilton A 

PROVIDER: S-EPMC6258900 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature