The potentiating effects of MDMA, MDE, MDA and cathinone on norepinephrine (noradrenaline, NE) and isoprenaline-evoked contractions in heart ventricular tissue were studied in isolated rat right ventricle. After eliciting a baseline NE-evoked response, each drug was applied to the tissue; MDMA (10 mcM), MDA (10 MuM), MDE (10 and 100 mcM) and cathinone (3 and 10 mcM), with 10 MuM cocaine serving as a comparison drug. The same procedures were used, but with the beta adrenergic agonist isoprenaline stimulating ventricular tissue rather than NE. When compared with vehicle, MDA, MDMA, cathinone and 100 mcM MDE, but not 10 mcM MDE, all increased the potency of NE-evoked contractions. MDA, MDMA, 10 mcM MDE, and cathinone did not attenuate or inhibit isoprenaline-evoked contractions. However, 100 mcM MDE reduced isoprenaline-evoked contractions. Study findings indicate that like cocaine, MDMA, MDE and cathinone potentiate NE-evoked contraction through competitive NE uptake inhibition, and not through acting on NE receptors. These findings are in agreement with findings showing that MDMA is an NE releaser and uptake inhibitor (e.g. Battaglia et al. 1989; Steele et al. 1987). On the basis of these study findings, the authors speculate that MDMA might increase risk of cardiac problems. Some cardiac problems have been reported (e.g. Dowling et al. 1987), yet it does not appear that MDMA use produces any greater risk of cardiac problems than other stimulants.