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Multiple Inhibitory Mechanisms of Lidocaine on Bradykinin Receptor Activity in Model Sensory Neurons
  1. Chika Hamaya, MD*,,
  2. Travis Barr, PhD*, and
  3. Gary R. Strichartz, PhD*
  1. *Department of Anesthesiology, Perioperative and Pain Medicine, Brigham & Women's Hospital, Boston, MA
  2. Department of Anesthesiology, Nishimino Kosei Hospital, Yoro, Gifu, Japan
  3. Molecular Oncology Research Institute, Tufts Medical Center, Boston, MA
  1. Address correspondence to: Gary R. Strichartz, PhD, Pain Research Center, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham & Women's Hospital, MRB611, 75 Francis St, Boston, MA 02115 (e-mail: gstrichartz{at}


Background and Objectives Local anesthetics (LAs) are often infiltrated subcutaneously for localized perioperative numbing. In addition to blocking nerve conduction, LAs act on pathways used by a variety of pain-inducing and inflammatory mediators. We describe the effects in isolated model sensory neurons of LAs on responses to the algogenic and sensitizing peptide, bradykinin (BK).

Methods ND/7 sensory neurons were stimulated by different concentrations of BK in the presence or absence of LAs, with transient increases in intracellular calcium (Δ[Ca+2]in) detected fluorometrically in fields of cells. Equilibrium saturable binding of radiolabeled BK also was conducted on the same type of cells, with and without LA.

Results Responses to low BK (5 nM) were inhibited by lidocaine at 1 mM (approximately 35% inhibition) and 10 mM (approximately 70% inhibition), whereas responses to high BK (100 nM) were unaffected by 1 mM yet inhibited (approximately 75%) by 10 mM lidocaine. Bupivacaine (1 and 2 mM) did not reduce peak Δ[Ca+2]in (using 5 nM BK). Lidocaine's quaternary derivative, QX-314 (10 mM), also was ineffective on peak Ca+2 (5 nM BK). Saturation binding of BK showed that lidocaine lowered the binding capacity (Bmax) without changing the KD, consistent with noncompetitive inhibition.

Conclusions At subclinical concentrations, lidocaine suppresses BK's activation of model sensory neurons. This effect adds to the known analgesic mechanisms of LAs and likely contributes to the reduction of postincisional pain.

  • bupivacaine
  • calcium
  • inflammation
  • lidocaine
  • local anesthetics
  • receptor binding

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  • Funding for this work was provided in part by the US Public Health Service, National Institutes of Health, from grants NIGMS R01-GM35647 and NIH/NCI R01-CA080153.

    The authors declare no conflict of interest.