beta-Endorphin and arginine vasopressin following stressful sensory stimuli in man.
This experimentation partially defines, for the first time, the response of beta-endorphin (ENDO) in man during tests designed to elicit nausea and motion sickness. These responses are similar to those associated with arginine vasopressin (AVP) and adrenocorticotropin (ACTH) to the extent that all hormones rise in response to motion sickness (p < 0.003). Repeated exposure diminished motion-induced release of ENDO (p < 0.005) and AVP (p < 0.004) despite a three-fold increase in resistance to motion stimuli. Higher post-stress levels of AVP (p < 0.04) and ACTH (p < 0.02) were correlated with greater resistance to motion sickness. These data support the hypothesis that release of AVP is a significant link between stressful motion and motion-induced nausea and other autonomic system changes. Further, resistant individuals apparently can tolerate higher peripheral levels of AVP before nausea results. Peripheral release of ENDO and ACTH may follow release of AVP; however, given the extensive and complex functional interactions that exist between AVP and the opiate systems, it is not yet possible to define a clear role for ENDO in the etiology of motion sickness.[1]References
- beta-Endorphin and arginine vasopressin following stressful sensory stimuli in man. Kohl, R.L. Aviation, space, and environmental medicine. (1992) [Pubmed]
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