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PNAS- Oct. 13, 1998
Minuscule amounts of nicotine&emdash;comparable to the trace amounts found in the blood after only fifteen minutes of exposure to second hand smoke&emdash;can trigger the release of chemicals that raise blood pressure in an animal model, report researchers from the University of Chicago in the October 13 issue of the Proceedings of the National Academy of Sciences.
Yan-Yi Peng, assistant professor of pharmacology and physiology, and Ying-Jun Cao, a postdoctoral researcher in Peng's lab, studied the effects of nicotine on the sympathetic nervous system of frogs, which is similar to its human counterpart. The sympathetic nervous system controls involuntary functions such as regulating blood pressure, temperature and the "fight or flight" reflex.
"This is the first time we have directly observed exactly what nicotine does to the nervous system," says Peng.
When Peng exposed frog neurons to minute doses of nicotine, they responded by releasing massive amounts of a neurotransmitter called lutenizing hormone-releasing hormone (LHRH).
Under normal circumstances, neurons release very low levels of LHRH. Under life-threatening conditions, such as a severe emergency, LHRH is released in abundance, signaling to other neurons to release a second neurotransmitter&emdash;norepinephrine (epinephrine in frogs). Norepinephrine constricts the arteries, thereby increasing blood pressure.
"It's shocking that such a small amount of nicotine caused a response that is usually seen only when the body is in a state of extreme emergency," says Peng.
"Because the frog and human nervous systems are so similar, our findings suggest that even the exceedingly small doses of nicotine we're working with in the lab can cause short-term high blood pressure, and perhaps over time, hypertension in humans," she explains.
But what is even more amazing to Peng, is that the release of LHRH is not mediated by any of the mechanisms known to govern the release of neurotransmitters. "In every other instance, calcium is required for neurotransmitter release. But for nicotine-induced LHRH release, calcium is totally unnecessary. In fact, calcium actually inhibited the release," Peng says .
To explain their baffling results, Peng has turned her attention to glial cells. Often described as "companion" cells to neurons, they form the insulating sheath that allows electrical impulses to travel from nerve to nerve.
"Researchers recently found that glial cells play more active roles than expected in neuronal information processing. They account for 90 percent of the cells in our brains," says Peng.
She speculates that these cells contain molecular pumps that normally collect LHRH so that neurons aren't overstimulated to release norepinephrine. "It is a way to maintain equilibrium," says Peng. Her preliminary research on glial cells suggests that nicotine may directly interfere with an LHRH pump.
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