PMID- 10978489
OWN - NLM
STAT- MEDLINE
DCOM- 20001023
LR  - 20190712
IS  - 0031-9384 (Print)
IS  - 0031-9384 (Linking)
VI  - 70
IP  - 1-2
DP  - 2000 Jul 1-15
TI  - Cardiovascular and sympathetic responses and reflex changes elicited by MDMA.
PG  - 141-8
AB  - The recreational use of 3,4-methylenedioxymethamphetamine (MDMA) has increased as 
      have the number of clinical reports linking MDMA use with cardiovascular 
      toxicity. Nonetheless, the cardiovascular and sympathetic nerve responses 
      elicited by MDMA have not been well characterized. The purpose of this study was 
      to characterize the mean arterial pressure (MAP), heart rate (HR), and renal 
      sympathetic nerve responses elicited by the acute administration of MDMA and to 
      determine whether neurotoxic doses of MDMA change cardiovascular and/or 
      cardiovascular reflex function. In conscious rats, MDMA or d-amphetamine elicited 
      similar dose-dependent increases in MAP. MDMA elicited significant bradycardia at 
      doses above 1.0 mg/kg. Pretreatment with phentolamine significantly reduced the 
      duration but not the magnitude of the pressor response elicited by MDMA. In 
      pentobarbital-anesthetized rats, MDMA (0.1 mg/kg) increased renal sympathetic 
      nerve activity (RSNA; 33 +/- 10%), while larger doses significantly decreased 
      RSNA (-91 +/- 3%, max). Neurotoxic doses of MDMA (20 mg/kg, s.c., b.i.d. for 4 
      days) significantly enhanced the bradycardic component of the Bezold-Jarisch 
      reflex elicited by i.v. serotonin when tested either 2 days or 2 weeks after the 
      last neurotoxic treatment. However, neurotoxic treatment did not significantly 
      affect baroreceptor reflex function. These results indicate that the acute 
      administration of MDMA and d-amphetamine produce similar cardiovascular and 
      sympathetic responses. Neurotoxic doses of MDMA can also significantly alter 
      cardiovascular reflex function. These findings raise the possibility that MDMA 
      may have the potential to produce cardiovascular and/or cardiac toxicity similar 
      to that elicited by other amphetamine analogs.
FAU - O'Cain, P A
AU  - O'Cain PA
AD  - Department of Pharmacology and Experimental Therapeutics, Louisiana State 
      University Health Sciences Center, 1901 Perdido St., New Orleans, LA 70112, USA.
FAU - Hletko, S B
AU  - Hletko SB
FAU - Ogden, B A
AU  - Ogden BA
FAU - Varner, K J
AU  - Varner KJ
LA  - eng
GR  - DA 08255/DA/NIDA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Physiol Behav
JT  - Physiology & behavior
JID - 0151504
RN  - 0 (Dopamine Uptake Inhibitors)
RN  - 0 (Serotonin Agents)
RN  - 333DO1RDJY (Serotonin)
RN  - CK833KGX7E (Amphetamine)
RN  - KE1SEN21RM (N-Methyl-3,4-methylenedioxyamphetamine)
SB  - IM
MH  - Amphetamine/pharmacology
MH  - Anesthesia
MH  - Animals
MH  - Baroreflex/drug effects
MH  - Blood Pressure/drug effects
MH  - Dopamine Uptake Inhibitors/pharmacology
MH  - Dose-Response Relationship, Drug
MH  - Heart Rate/drug effects
MH  - Hemodynamics/*drug effects
MH  - Male
MH  - N-Methyl-3,4-methylenedioxyamphetamine/*pharmacology/toxicity
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reflex/*drug effects
MH  - Serotonin/pharmacology
MH  - Serotonin Agents/*pharmacology/toxicity
MH  - Sympathetic Nervous System/*drug effects
EDAT- 2000/09/09 11:00
MHDA- 2001/02/28 10:01
CRDT- 2000/09/09 11:00
PHST- 2000/09/09 11:00 [pubmed]
PHST- 2001/02/28 10:01 [medline]
PHST- 2000/09/09 11:00 [entrez]
AID - S0031-9384(00)00235-3 [pii]
AID - 10.1016/s0031-9384(00)00235-3 [doi]
PST - ppublish
SO  - Physiol Behav. 2000 Jul 1-15;70(1-2):141-8. doi: 10.1016/s0031-9384(00)00235-3.