ArticleThe Journal of physiology2001
Bradykinin evokes a Ca2+-activated chloride current in non-neuronal cells isolated from neonatal rat dorsal root ganglia.
Article in The Journal of physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 26 citations in OpenAlex.
- Peripheral Inflammatory Hyperalgesia Depends on P2X7 Receptors in Satellite Glial Cells.Frontiers in physiology · 2020Article
- Involvement of bradykinin in brain edema development after ischemic stroke.Pflugers Archiv : European journal of physiology · 2015Review
- Bradykinin-induced chemotaxis of human gliomas requires the activation of KCa3.1 and ClC-3.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Calcitonin gene-related peptide-mediated enhancement of purinergic neuron/glia communication by the algogenic factor bradykinin in mouse trigeminal ganglia from wild-type and R192Q Cav2.1 Knock-in mice: implications for basic mechanisms of migraine pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- The voltage-gated sodium channel Na(v)1.9 is an effector of peripheral inflammatory pain hypersensitivity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Bradykinin decreases K(+) and increases Cl(-) conductances in vagal afferent neurones of the guinea pig.The Journal of physiology · 2004Article
- Indirect actions of bradykinin on neonatal rat dorsal root ganglion neurones: a role for non-neuronal cells as nociceptors.The Journal of physiology · 2001Article
- Bradykinin evokes a Ca2+-activated chloride current in non-neuronal cells isolated from neonatal rat dorsal root ganglia.The Journal of physiology · 2001Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
We have studied the effect of bradykinin (Bk) on fibroblast-like satellite (FLS) cells isolated from cultures of neonatal rat dorsal root ganglia (DRG). In voltage-clamped FLS cells Bk evoked an inward current response that was concentration dependent with a half-maximal concentration of 2 nM. In indo-1 AM-loaded FLS cells Bk evoked a rise in intracellular Ca2+ that was concentration dependent with a half-maximal concentration of 1 nM. The FLS cells still produced an inward current in response to Bk in the absence of extracellular Ca2+ but the response was inhibited if the intracellular concentration of EGTA was increased from 0.5 to 5 mM, which suggests that the inward current was dependent on the release and subsequent rise of intracellular Ca2+. The reversal potential of the Bk-induced inward current was consistent with the current being due to an increase in Cl- conductance and shifted in a Nernstian manner when the intracellular Cl- concentration was reduced. The inward current response to Bk was blocked by the B2 receptor antagonist HOE-140, which indicates that the response was due to activation of B2 receptors. The data suggest that Bk evokes a rise in intracellular Ca2+ and activation of a Ca2+-activated Cl- conductance in the FLS cells and raise the possibility that FLS cells contribute to the pro-inflammatory effects of Bk in DRG.
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