Key result
Psychological stress triggers marked blood pressure and heart rate increases in rats via sympathetic hyperactivity.
A novel open-field stress model in freely moving rats demonstrates that psychological novelty stress induces marked cardiovascular effects mediated by sympathetic hyperactivity.
Should not change clinical practice; hypothesis-generating for sympathetic mechanisms in human stress-related cardiovascular disease.
We developed a new model of psychological "open-field" stress in freely moving rats. Blood pressure and heart rate of the rats were measured by radiotelemetry and behavior analyzed by video tracking software. Open-field exposure induced marked increases in blood pressure and heart rate. Repeated daily exposure induced pressor responses that were slightly higher on Day 4 when compared to Day 1. Pretreatment with the beta1-adrenoceptor antagonist atenolol inhibited the tachycardia whereas the ganglion blocker pentolinium inhibited the pressor response, indicating involvement of the sympathetic nervous system. Pretreatment with diazepam prevented the novelty stress-induced pressor response and reduced the tachycardia. These results show that the psychological stress of exposing rats to an open field induces marked cardiovascular effects that are mediated by sympathetic hyperactivity. This model is unique in that it focuses on psychological stress and allows concomitant measurement of blood pressure, heart rate, and behavior in freely moving rats.
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Buuse et al. (2001) studied Psychological stress. Psychological 'open-field' stress was evaluated on Blood pressure and heart rate. Psychological stress from open-field exposure in freely moving rats induced marked increases in blood pressure and heart rate that were mediated by sympathetic hyperactivity.
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