This paper summarizes and describes two lines of research into the effects of MDMA and metabolites on arginine vasopressin (AVP) release. Findings described here have appeared in previously published reports by the same authors (Henry et al. 1998; Forsling et al. 2001; 2002). In one study, eight male MDMA-naive volunteers were given 40 mg MDMA, and in another study, MDMA or one of 5 metabolites was applied to rat hypothalamus. Substances tested were racemic MDMA, R-(-)-MDMA, S-(+)-MDMA, DHMA, DHA, HMMA, HMA, racemic MDA and each enantiomer of MDA, given at 0.1, 10 or 1000 mcg, and enantiomers at 500 mcg. Racemic MDMA (500 mcg) was also tested in combination with 500 mcg of racemic HMMA, a major metabolite. As reported in previously published papers, MDMA was associated with AVP release in humans, even at this relatively low dose. AVP release was uncorrelated with cortisol release, which was more strongly influenced by circadian rhythms than by MDMA at this low dose. AVP release was inversely related to plasma MDMA concentrations in the first hour after drug administration. MDMA and four of the five metabolites stimulated AVP release in rat hypothalamic cultures, with DHMA being the only exception. S-(+)-MDMA stimulated more AVP release in hypothalamus than R-(-)MDMA, and HMMA was more effective than MDMA in stimulating AVP release. After examining findings from both studies, the authors conclude that both MDMA and at least some of its metabolites play a role in release of AVP after drug administration, and that the drug-induced release of AVP may be associated with ecstasy-induced hyponatremia in humans.