In this study the hypothesis that hypnotic analgesia under conditions of stress is mediated through a neurochemical mechanism involving the release of opioid peptides in the CNS was investigated. Ten highly hypnotizable subjects participated in a 2 x 2 factorial design, which involved hypnotic analgesia, stress and double blind administration of naloxone (an opiate antagonist) or placebo. Analysis of post-hypnosis results indicates that hypnotic analgesia was significantly reversed by the interactive effects of stress and naloxone. It is inferred that stress may be the common psychological denominator of the various analgesic methods which effectively engage this endogenous pain inhibitory system. Additional analyses of anxiety measures reveals no significant association between trait and state anxiety, but significant relationships between state anxiety and time tolerance to ischemic pain. These results suggest that anxiety remains a definitional problem and that previous conceptualizations may not have satisfactorily explained the affect's adaptive function.