DALLAS - March 5, 2002 - Researchers at UT Southwestern Medical Center at Dallas have identified the underlying mechanism by which cocaine triggers hypertensive crisis, the most severe form of high blood pressure and one of the most common cocaine-related, cardiovascular emergencies in the United States.
The findings, reported in todays issue of Circulation, may lead to the development of new treatment strategies for cocaine-induced blood pressure elevation and related complications including stroke and acute myocardial infarction.
The underlying mechanism of the blood-pressure-raising effect of cocaine use in humans has not been well studied, said Dr. Wanpen Vongpatanasin, senior author of the study and assistant professor of internal medicine. Most of us believe that cocaine increases blood pressure mainly by preventing clearance or reuptake of noradrenaline from blood vessels into the nerve endings and the excess levels of noradrenaline cause blood vessels to constrict. However, we found that this mechanism plays a very small role in humans. Instead, cocaine increases blood pressure by stimulation of the heart to cause rapid heartbeat and increased cardiac output. This elevation in blood pressure, if severe or persistent, can lead to damage of multiple vital organs such as the heart, brain and kidney.
Approximately 25 million Americans have tried cocaine, and the drug is the most frequent cause of drug-related deaths reported by medical examiners. In 1999, cocaine use was cited in 30 percent of all drug-related emergency department visits and cocaine is the most commonly used illicit drug among people seeking care in hospital emergency departments or drug treatment centers.
The textbook explanation of cocaine-related elevated blood pressure is based on evidence from previous studies in rats and mice, said Dr. Meryem Tuncel, lead author of the study and a postdoctoral fellow in hypertension. However, anesthesia used to sedate th
Contact: Amy Shields
UT Southwestern Medical Center