Influence of amygdala lesions on cardiovascular responses to alerting stimuli, on behaviour and on blood pressure development in spontaneously hypertensive rats.

Spontaneously hypertensive rats (SHR), and often also humans genetically predisposed to hypertension, exhibit cardiovascular hyperreactivity to alerting stimuli, which derives from limbic-hypothalamic levels and seems important for inducing primary hypertension. It is further known that the limbic amygdala complex normally reinforces emotionally induced defence reactions. The amygdala were therefore bilaterally destroyed in 6 week old SHR, and compared with sham-operated SHR concerning development of hypertension, cardiovascular reactivity to environmental stimuli and explorative behaviour. When related to controls, the arterial pressure elevation was significantly attenuated in the amygdalalesioned SHR, though their pressure was nevertheless raised 40% at 6 months of age. Concerning cardiovascular responsiveness to mild environmental stimuli the groups did not differ; neither concerning explorative behaviour nor in general motor activity. However, the amygdala-lesioned SHR responded decidely less than controls to stressful, fear-inducing stimuli. The amygdala complex may therefore play an important role in aggravating SHR hypertension by reinforcing defence reactions to stressful influences, when such stimuli are at hand. However, according to the present study the amygdala nuclei are not the origin of the centrally determined cardiovascular hyperreactivity, which in SHR seems decisive for inducing hypertension.