Characterization of the Cardiovascular and Sympathetic Nerve Fesponses Elicited by "Ecstasy"
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A new group of amphetamine analogues, including 3, 4 methylenedioxymethamphetamine (MDMA or "Ecstasy"), has recently emerged onto the drug scene. Although rumored to be a "safe" drug that promotes emotional closeness and serenity, MDMA has been shown to influence cardiovascular function and produce cardiovascular toxicity. The spectrum of the cardiovascular response elicited by MDMA and the mechanism(s) responsible are unknown. Therefore, the purpose of this study was to provide the first complete characterization of the dose-response relationships of MDMA (0.01-3.0 mg/kg i.v.) for heart rate and arterial pressure In conscious rats, and sympathetic nerve activity in pentobarbital-anesthetized rats. This characterization will provide strategies to elucidate the mechanism(s) responsible for the toxicities associated with MDMA abuse. Dose-response relationships for cocaine and amphetamine (0.01-3.0 mg/kg i.v.) were also performed for reference. Cocaine, amphetamine, and MDMA all elicited similar dose-dependent increases in blood pressure and tachycardia (increases in heart rate) at low doses and bradycardia (decreases In heart rate) at high doses. In anesthetized rats, MDMA produced dose-dependent decreases in renal sympathetic nerve activity (max. depression -91% ±3). The sympathetic nerve activity responses were similar in magnitude to those previously shown to be elicited by cocaine and amphetamine. From these data we concluded that MDMA's effects are most likely mediated by mechanism(s) similar to those responsible for the cardiovascular and sympathetic nerve responses elicited by cocaine and amphetamine.