Nov. 18, 2010 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 vigorous sprint. This type of pain
is called "ischemic" pain and is sensed in the body by receptors
on sensory neurons. It has been suggested that lactic acid,
which increases during muscle exertion under conditions where
oxygen is low, is a potential mediator of ischemic 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 ischemic muscle,
adenosine tri-phosphate (ATP), works together with acid by
increasing the sensitivity of ASIC3 on sensory neurons."
Importantly, ATP levels have been shown to rise