Vascular actions of MDMA involve α1 and α2‐adrenoceptors in the anaesthetized rat
John Mcdaid, James R. Docherty
British Journal of Pharmacology June 1, 2001 DOI: 10.1038/sj.bjp.0704094 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Experimental study Peer reviewed |
|---|---|
| Population | Pithed and pentobarbitone anesthetized rats |
| Interventions | MDMA prazosin yohimbine methiothepin ritanserin methoxyidazoxan cocaine |
| Dose | MDMA 1 and 5 mg kg-1; prazosin 0.1 mg kg-1; yohimbine 1 mg kg-1; methiothepin 0.1 mg kg-1; ritanserin 1 mg kg-1; methoxyidazoxan 0.1 mg kg-1; cocaine 1 and 10 mg kg-1 |
| Topics | MDMA |
| Keywords | Ritanserin Prazosin Yohimbine Endocrinology Ketanserin Pharmacology Adrenergic antagonist Receptor antagonist |
| Citations | 46 |
| Key findings | MDMA's cardiovascular effects in rats involve distinct adrenoceptor mechanisms: initial pressor response via α₂- and possibly α₁-adrenoceptors and 5-HT₂ receptors, a 1-minute pressor component largely α₁-mediated, and a sustained depressor response involving α₂-adrenoceptors. |
Abstract
We have investigated the effects of methylenedioxymethamphetamine (MDMA, ‘ecstasy’), i.v., on diastolic blood pressure (DBP) in pithed and pentobarbitone anaesthetized rats. In pithed rats, the non‐selective 5‐HT receptor antagonist methiothepin (0.1 mg kg −1 ) and the α 2 ‐adrenoceptor antagonists methoxyidazoxan and yohimbine (1 mg kg −1 ) showed significant α 1 ‐adrenoceptor antagonist potency, but methiothepin did not show α 2 ‐adrenoceptor antagonist potency. MDMA (1 and 5 mg kg −1 ) produced pressor responses which were significantly reduced by the α 1 ‐adrenoceptor antagonist prazosin (0.1 mg kg −1 ), yohimbine (1 mg kg −1 ) or methiothepin (0.1 mg kg −1 ), but not by the 5‐HT 2 receptor antagonist ritanserin (1 mg kg −1 ). In anaesthetized rats, antagonists revealed two phases with three components to the effects of MDMA (5 mg kg −1 ) on DBP: an initial pressor response, a later pressor component at 1 min, the sustained depressor response. Methoxyidazoxan, methiothepin or the combination ritanserin/prazosin significantly reduced the initial pressor response, although neither of the latter compounds alone had any effect. The pressor response to MDMA (5 mg kg −1 ) at 1 min was converted to a depressor response by prazosin and to a lesser extent methiothepin and methoxyidazoxan. The depressor response to MDMA (5 mg kg −1 ) was significantly reduced by methoxyidazoxan (0.1 mg kg −1 ), and by the noradrenaline re‐uptake blocker cocaine 10 mg kg −1 but not 1 mg kg −1 . However, the most marked reduction in the depressor response was produced by the combination of methoxyidazoxan and cocaine. It is concluded that the initial pressor response to MDMA (5 mg kg −1 ) in anaesthetized rats involves α 2 ‐ and possibly α 1 ‐adrenoceptors and 5‐HT 2 receptors, the pressor component at 1 min is largely α 1 ‐adrenoceptor mediated, and the sustained depressor response involves α 2 ‐adrenoceptors. British Journal of Pharmacology (2001) 133 , 429–437; doi: 10.1038/sj.bjp.0704094
Comparable studies
Other preclinical and animal studies on MDMA, most cited first.
Citations in the library
Cited by 14
- Which neuroreceptors mediate the subjective effects of MDMA in humans? A summary of mechanistic studies Human Psychopharmacology: Clinical and Experimental December 1, 2001
- The Norepinephrine Transporter Inhibitor Reboxetine Reduces Stimulant Effects of MDMA (“Ecstasy”) in Humans Clinical Pharmacology & Therapeutics June 15, 2011
- Acute Psychological and Neurophysiological Effects of MDMA in Humans Journal of Psychoactive Drugs June 1, 2002
- The role of monoamines in the changes in body temperature induced by 3,4‐methylenedioxymethamphetamine (MDMA, ecstasy) and its derivatives British Journal of Pharmacology March 3, 2010
- Effects of MDMA, MDA and MDEA on blood pressure, heart rate, locomotor activity and body temperature in the rat involveα‐adrenoceptors British Journal of Pharmacology February 20, 2006
and 9 more in the library
Cites 11
- 3,4-Methylenedioxymethamphetamine and 3,4-methylenedioxyamphetamine destroy serotonin terminals in rat brain: quantification of neurodegeneration by measurement of [3H]paroxetine-labeled serotonin uptake sites. Journal of Pharmacology and Experimental Therapeutics September 1, 1987
- 'Eve' and 'Ecstasy'. A report of five deaths associated with the use of MDEA and MDMA JAMA March 27, 1987
- The Psychological and Physiological Effects of MDMA on Normal Volunteers Journal of Psychoactive Drugs October 1, 1986
- 'Eve' and 'Ecstasy' JAMA March 27, 1987
- In vivo evidence for free radical involvement in the degeneration of rat brain 5‐HT following administration of MDMA (‘ecstasy’) and p‐chloroamphetamine but not the degeneration following fenfluramine British Journal of Pharmacology July 1, 1997
and 6 more in the library