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Angina sufferers everywhere know the feeling all too well: a tight, twitching
pain in the chest after a stressful day. A piercing burn during a morning jog.
Or, worse, the breathtaking stab that signals an impending heart attack.
Here at the Why Files, our tickers beat a little faster just thinking about it. After all, more than a million Americans will have a heart attack this year, according to the American Heart Association. But take comfort. Heart pain, like other body aches, is a valuable service provided by your body's network of watchdog nerve cells.
As this Why File reports, scientists have just gotten a closer look at the pain cells in your precious pump. What they saw might surprise you.
When arteries are clogged, precious oxygen-harboring blood from the lungs squeezes through at a trickle instead of a gush, often resulting in a condition known as ischaemia (oxygen deprivation). In response, the heart releases a flood of chemicals that dilate the blood vessels and send you that precious warning that your heart's in trouble: pain.
One mediator of this pain may be the same receptors, found all over the skin and tongue, that ignite when you encounter something hot. The receptors have now been found in the heart, Penn State physiologist Hui-Lin Pan reported in a recent issue of the Journal of Physiology.
The receptors are most famous, perhaps, for their response to the searing "heat" you sense after devouring a chili pepper. Capsaicin, the pungent chemical in peppers, binds to the receptor and sets them aflame. (Why these receptors react with such fury to a harmless chemical is another story entirely.)
"Almost twenty years ago, it was found that when you applied capsaicin to the heart, it triggered blood pressure and heart rate changes" similar to those seen during a heart attack, says Pan. But nobody knew what receptors, on which cells, were doing the work.
To find out, Pan and his colleagues bathed rat hearts with a chemical marker designed to bind specifically to the capsaicin receptors found on cells elsewhere in the body. (It's prettier than it sounds. Under a special microscope, the marker fluoresces wherever the receptor exists.) Pan says some scientists had doubts about the possibility of capsaicin receptors in the heart -- after all, what use would a warning system for heat and habaneros have in the heart?
Plenty, apparently.
"The receptors were all over the surface of the heart," Pan says. But "what was really surprising was that they were only located superficially." There appear to be no such receptors inside the heart, which Pan says could explain why some people suffer so-called silent ischaemia. People with this problem -- often diabetics -- experience a lack of oxygen in the heart but feel no pain.
A microscopic
image of a rat's left ventricle. The green fluorescence shows the presence
of capsaicin receptors -- the same receptors that respond to heat and chili
peppers on the skin and tongue -- on the surface of the heart. Image courtesy
Hui-Lin Pan
The discovery of capsaicin receptors on the heart begged another question, Pan says. Since they play such a critical role in pain messages elsewhere in the body, it makes sense that the receptors could act similarly in the heart. But do they?
"The rats can't tell us when they experience pain," Pan notes. "So we can't study chest pain directly. Instead, we studied the reflex by looking at blood pressure as an indirect measure of chest pain."
The researchers treated one group of rats with a noxious relative of capsaicin -- in effect, crippling the animals' capsaicin receptors. Another group of rats was treated with a placebo drug that left the receptors in working order. Then Pan and his team doused both groups with a chemical, called bradykinin, that the body produces in response to ischaemia.
As expected, the researchers watched blood pressure skyrocket in the rats with normal capsaicin receptors. But the rats with "knocked out" receptors barely blinked -- and their blood pressure levels stayed constant.
"Initially, we thought if the receptor was knocked out, maybe there would be another type of receptor also present, and that we'd see a partial effect," says Pan. "What was really surprising is that without these receptors, you achieve no effect at all."
No one can be sure whether, or to what extent, the nerve cells bearing capsaicin receptors are involved in heart pain or heart attacks, Pan notes. Using bradykinin to simulate ischaemia is one thing; actual ischaemia is another. But the study adds flames to an already burning suspicion, and Pan says his next project will be to induce ischaemia in rats and watch the receptors in real-world action.
In the long run, Pan's work may "provide new insight into ways of managing cardiac pain... and it could help improve cardiac survival from cardiac infarctions," otherwise known as heart attacks, says Harold Schultz, a professor of physiology at the University of Nebraska Medical Center.
For instance, people with chronic heart pain may be treated with drugs that block -- or at least impair -- the receptors that send pain messages to the brain.
For now, it's too early to say with certainty whether the capsaicin receptors are in fact responsible. And Schultz cautions that blocking the signal entirely might not be the best way to treat heart pain, since it so often is the only warning sign before a heart attack.
What's more, "these sensory nerves are beneficial to the heart because they liberate chemicals when they are stimulated that help protect cardiac tissue from injury during ischemia," Schultz points out. "So the ultimate goal is to be able to manage the pain perception to tolerable levels while allowing the protective function of these nerve endings to proceed during ischemia."
It's important, Schultz notes, to keep the bigger picture in mind. Decoding the messages passed between body and the brain has long been one of medicine's most puzzling tasks. Until now, it seems, the heart has been hiding one hot little secret.
-- Sarah Goforth
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