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It takes 2: Double detection key for sensing muscle pain
When cardiac or skeletal muscle is not receiving enough oxygen to meet metabolic demands, a person will experience pain, such as angina, chest pain during a heart attack, or leg pain during a vigourous sprint. This type of pain is called 'ischaemic' pain and is sensed in the body by receptors on sensory neurones. It has been suggested that lactic acid, which increases during muscle exertion under conditions where oxygen is low, is a potential mediator of ischaemic pain via action at acid sensing channel 3 (ASIC3). However, the acid signal it generates is quite subtle and is unlikely to act alone.
'In our study, we examined whether other compounds that appear during ischemia might work synergistically with acid upon ASIC3,' explains senior study author, Dr Edwin W. McCleskey. 'We found that another compound released from ischaemic muscle, adenosine tri-phosphate (ATP), works together with acid by increasing the sensitivity of ASIC3 on sensory neurones.' Importantly, ATP levels have been shown to rise rapidly outside ischaemic muscle cells and synergistic action of ATP and acid has been observed in animal models of ischaemia.
The researchers went on to show that ATP binds to a membrane purine receptor, called P2X, and that P2X and ASIC appear to form a molecular complex that serves to sensitise ASIC to acid. 'Taken together, our results help to explain the paradox that acid appears incapable of triggering ischaemic pain by itself yet buffering acid severely decreases sensory detection of ischaemic pain,' concludes Dr McCleskey. 'ATP, which is released from oxygen-deprived contracting muscle, increases the ability of ASICs to respond to a slight decrease in pH.'
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