Central nucleus of the amygdala and the development of hypertension in spontaneously hypertensive rats.

Abstract

Electrolytic lesions of the central nucleus of the amygdala (ACe) have been shown to attenuate the development of hypertension in spontaneously hypertensive rats (SHR). Whether this was due to destruction local neurons and/or fibres of passage is unknown. In the present study, neuronal perikarya in the ACe of 4 week-old SHR were selectively destroyed with ibotenic acid. Three separate experiments were conducted, in which mean arterial pressure (MAP), heart rate and blood pressure responses to acute mental stress were measured in groups of lesioned and sham-lesioned SHR. In Experiment 1, in which rats were fed ad lib., lesioned SHR had a significantly lower average MAP (173 mmHg $\pm$ 7 S.E.) vs. sham-lesioned SHR (201 $\pm$ 4), 15 weeks post-operation (p 0.05, t-test). These results show that the attenuation of the development of hypertension in young SHR is due to the selective destruction of neurons in the ACe. The lesioned animals in Experiment 1 also had significantly lower body weights (BW) from 5 weeks post-operation onwards (p 0.5, two-way repeated-measures ANOVA). Therefore, in Experiment 2, food intake (and hence BW) among the lesioned and sham-lesioned rats was equalized. Average MAP in the lesioned SHR at 7 and 15 weeks post-operation was not different vs. sham-lesioned SHR, but was significantly higher (190 $\pm$ 9) vs. sham-lesioned SHR (164 $\pm$ 5) 22 weeks post-operation (p 0.05, t-test). These results indicate that destruction of neuronal perikarya in the ACe in young SHR merely delays the development of hypertension, due to a reduced BW gain. In Experiment 3, the effect of a high salt diet in ACe-lesioned SHR was examined. No significant differences in MAP were measured between lesioned and and sham-lesioned rats 4 or 11 weeks post-operation.