People in the throes of a heart attack usually experience a burning chest pain. Scientists appear to have pinpointed the cause of that pain: It turns out that heart tissue contains the same cell-surface protein that triggers a sensation of fiery pain when the skin becomes too hot or when the tongue tastes chili peppers.
The protein, vanilloid receptor 1 (VR1), sits on nerve cells. In the skin, the receptor produces pain signals in response to heat. In the tongue, it also responds to capsaicin, a compound in chilies and some spices (SN: 11/8/97, p. 297).
The outermost layer of the rat heart also displays VR1, Hui-Lin Pan of Pennsylvania State University College of Medicine in Hershey and his colleagues report in the Sept. 1 Journal of Physiology. Moreover, when capsaicin or another chemical called bradykinin was applied to the hearts of rats, the animals’ blood pressure and heart-nerve activity increased in a manner similar to that seen in heart attacks. Bradykinin is one of the compounds released by oxygen-starved heart tissue and is thought to mediate the initial symptoms of a heart attack.
People with chronic chest pain caused by angina could benefit from drugs that block the activation of the heart VR1, Pan and his colleagues suggest.
The scientists also point out that the absence of VR1 from the inner layers of the heart may help explain so-called silent ischemia, episodes in which people experience heart attacks without pain or other symptoms.
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