ArticleThe Journal of physiology2004
Bradykinin decreases K(+) and increases Cl(-) conductances in vagal afferent neurones of the guinea pig.
Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 47 citations in OpenAlex.
- Role of TRP channels in GAmerican journal of physiology. Lung cellular and molecular physiology · 2020Article
- Molecular/Ionic Basis of Vagal Bronchopulmonary C-Fiber Activation by Inflammatory Mediators.Physiology (Bethesda, Md.) · 2020Review
- Targeting C-fibers for peripheral acting anti-tussive drugs.Pulmonary pharmacology & therapeutics · 2019Review
- TMEM16B determines cholecystokinin sensitivity of intestinal vagal afferents of nodose neurons.JCI insight · 2019Article
- Depolarizing Effectors of Bradykinin Signaling in Nociceptor Excitation in Pain Perception.Biomolecules & therapeutics · 2018Review
- Mechanisms of pruritogen-induced activation of itch nerves in isolated mouse skin.The Journal of physiology · 2017Article
- The volume-regulated anion channel (LRRC8) in nodose neurons is sensitive to acidic pH.JCI insight · 2017Article
- Vagal Afferent Innervation of the Airways in Health and Disease.Physiological reviews · 2016Review
- Peripheral neural circuitry in cough.Current opinion in pharmacology · 2015Review
- Targeting peripheral afferent nerve terminals for cough and dyspnea.Current opinion in pharmacology · 2011Review
- Ionic mechanisms underlying inflammatory mediator-induced sensitization of dural afferents.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- The acute nociceptive signals induced by bradykinin in rat sensory neurons are mediated by inhibition of M-type K+ channels and activation of Ca2+-activated Cl- channels.The Journal of clinical investigation · 2010Article
- Central regulation of the cough reflex: therapeutic implications.Pulmonary pharmacology & therapeutics · 2009Review
- Peripheral mechanisms of pain and analgesia.Brain research reviews · 2009Review
- Review
- Review
- Bradykinin-induced chloride conductance in murine proximal tubule epithelial cells.Molecular and cellular biochemistry · 2007Article
- Calmodulin contributes to gating control in olfactory calcium-activated chloride channels.The Journal of general physiology · 2006Article
- Caged vanilloid ligands for activation of TRPV1 receptors by 1- and 2-photon excitation.Biochemistry · 2006Article
- Role of chloride channels in bradykinin-induced guinea pig airway vagal C-fibre activation.The Journal of physiology · 2005Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Bradykinin (BK) is an inflammatory mediator that can excite and sensitize primary afferent neurones. The nature of the ionic channels underlying the excitatory actions of BK is still incompletely understood. Using whole-cell patch-clamp recording from acutely dissociated nodose ganglion neurones (NGNs) we have examined the ionic mechanism responsible for BK's excitatory effect. Bath-applied BK (0.1 microM) depolarized the membrane potential (29 +/- 3.1 mV, n= 7), evoked action potentials, and induced an inward ionic current (I(BK)) with two distinctive membrane conductances (g(m)). Initially, g(m) decreased; the ionic current associated with this g(m) had a reversal potential (E(rev)) value of -87 +/- 1.1 mV (n= 26), a value close to E(K) (-89 mV). Subsequently, g(m) increased; the ionic current associated with this g(m) had an estimated E(rev) of 49 +/- 4.3 mV (n= 23). When the second component was isolated from the first component, by replacing [K(+)](o) with Cs(+), E(rev) was 20 +/- 4.7 mV (n= 10). Replacing external NaCl with NMDG-Cl or choline-Cl, or reducing [Ca(2+)](o) did not significantly diminish I(BK). After replacing external NaCl with sodium isethionate, E(rev) for the second component shifted to 56 +/- 8.8 mV (n= 4), a value close to the E(Cl) (66 mV). The second component was inhibited by intracellular BAPTA or by bath application of niflumic acid (100 microM), a Ca(2+)-activated Cl(-) channel blocker. These results suggest that the first and second components of I(BK) are produced by a decrease in K(+) conductance and an increase in Ca(2+)-activated Cl(-) conductance, respectively. The BK-evoked Cl(-) conductance in NGNs may be the first demonstration of an inflammatory mediator exciting primary afferents via an anion channel.
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