The role of central nervous system arginine vasopressin (AVP) and oxytocin (OXY) in the cardiovascular response to acute stress was examined using three experimental models: pharmacological antagonism of central AVP-OXY receptors; lesions of the paraventricular nucleus (PVN); and rats genetically lacking in AVP synthesis, i.e., the Brattleboro strain. Central administration of an AVP-OXY antagonist abolished the increase in heart rate (HR) seen following acute footshock stress. The group receiving centrally administered antagonist increased HR 15 ± 17 (SE) beats/min, whereas, in contrast, the group receiving intravenous administration of the antagonist showed a 66 ± 17 beats/min increase, and the group receiving intraventricular antagonist vehicle showed a 101 ± 14 beats/min increase in response to stress. In a second study, electrolytic lesions of the PVN also blocked the increase in HR seen following stress, 20 ± 12 beats/min for PVN-lesioned rats, 74 ± 25 beats/min for sham lesion rats, and 93 ± 7 beats/min for rats with a lesion not destroying the PVN. In the final study, the responses of Brattleboro rats, i.e., rats genetically deficient in vasopressin synthesis, were equivalent to their Long-Evans controls (131 ± 13 and 147 ± 12 beats/min, respectively). In each of these studies, the blood pressure responses to the stressor were equivalent for control and experimental groups. The results of these studies suggest that a neuropeptide system originating in or passing through the PVN may play an important role in the cardiovascular responses to stress and further suggest that the central OXY system may be one pathway mediating this response.
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|State||Published - 1989|