“…Several membrane ion channels and receptors have been identified as targets of various VAs (Rudolph and Antkowiak, 2004;Hemmings et al, 2005). Enhancement of the activity of inhibitory ionotropic receptors (Lobo and Harris, 2005;Zeller et al, 2008), depression of the excitatory ionotropic receptors (Yamakura et al, 2001), potentiation of the 2P-domain K + channels (Patel and Honore, 2001), inhibition of voltage-gated Na + channels (Hemmings, 2009) and of the transient receptor potential (TRP) family member TRPC5 (Bahnasi et al, 2008) probably all contribute to the central clinically relevant anaesthetic effects, whereas the action of the same VAs on other ion channels might, at least in part, be responsible for their numerous adverse effects (Stachnik, 2006;Bovill, 2008). Indeed, activation of TRP member TRPA1 by the 'pungent' VAs (those that are known to excite peripheral nociceptive neurons), isoflurane and desflurane Cornett et al, 2008;Eilers et al, 2010), and sensitization of TRPV1 to its agonists, capsaicin and protons Eilers et al, 2010), might contribute to postoperative pain and inflammation, as well as producing airway irritation.…”