6. Conclusion

The ASIC family is a potential target for new analgesics. In rheumatoid arthritis and vascular ischemia, as well as in the routine perioperative settings, inflammation and ischemic pain conditions are a sign mark of acidic nociception which can be reduce by the NSAIDs and by direct inhibition of sensory neuron ASIC current [77].

Work is currently in progress on a more selective and potent ASIC blocker and could potentially be an effective agent in the treatment of inflammatory and ischemic acute or chronic pain in the future [78]. Key regulators of membrane excitability are inflammatory mediators and key receptors (kinins, mPGEs), ion channels (TRPV1, NaV 1.7), and neurotrophins (NGF). Similarly, α(2A)-adrenoceptor agonists also proven to be effective in various pain conditions, in the spinal dorsal horn, by inhibitory action on α(2A)-adrenoceptors on central terminals of primary afferent nociceptors (presynaptic inhibition), by direct α2-adrenergic action on spinal pain-relay neurons (post-synaptic inhibition) noradrenaline released from descending pathways originating in the pontine A5–A7 cell groups decreases pain and by α1-adrenergic activation of inhibitory interneurons. Furthermore, α(2C)-adrenoceptors on axon terminals of excitatory interneurons might subsidize to spinal control of pain [79]. These targets are currently under work to establish new analgesics with minimum side effects as exhibited by the currently used COX inhibitors.
