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ASIC3: a lactic acid sensor for cardiac pain
1Vollum Institute, Oregon Health & Science University, Portland, OR 97201-3098, USA. immked@ohsu.edu
Thescientificworldjournal
|June 14, 2003
Summary
Vasoocclusive pain, like angina, is triggered by insufficient blood flow causing ischemia. Sensory neurons in the heart possess an ion channel specifically activated by lactic acid, a byproduct of this ischemia.
Area of Science:
- Cardiology
- Neuroscience
- Pain Research
Background:
- Vasoocclusive pain, exemplified by angina, arises from inadequate blood supply to tissues, leading to ischemia.
- Conditions such as heart attack, sickle cell anemia, and peripheral artery disease involve vasoocclusive pain.
- Ischemia forces cells into anaerobic metabolism, releasing lactic acid.
Purpose of the Study:
- To investigate the role of specific ion channels in sensory neurons related to ischemia-induced pain.
- To understand the molecular mechanisms underlying the detection of lactic acid by cardiac sensory neurons.
Main Methods:
- Analysis of sensory neurons innervating the heart.
- Investigation of ion channel function in response to ischemic conditions and lactic acid.
Main Results:
- Sensory neurons in the heart are densely equipped with a specific ion channel.
- This ion channel is activated by lactic acid, a key mediator of ischemic pain.
- The channel is precisely tuned to detect the levels of lactic acid produced during muscle ischemia.
Conclusions:
- Lactic acid released during muscle ischemia acts as a direct stimulus for sensory neurons in the heart.
- This finding provides a novel molecular target for understanding and potentially treating vasoocclusive pain, including angina.