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

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 of local neurons and/or fibers is unknown. In the present study, neuronal perikarya in the ACe of 4-wk-old SHR were selectively destroyed with ibotenic acid. In two experiments, each comprising lesioned and sham-lesioned SHR, mean arterial blood pressure (MAP) was measured 7 and 15 wk after operation in the second experiment also at 22 wk. In the first experiment, in which rats were fed ad libitum, lesioned SHR had significantly lower body weights from 5 wk postoperation onward, and at 15 wk postoperation their average MAP [173 +/- 7 mmHg (SE)] was significantly lower vs. sham-lesioned SHR (201 +/- 4 mmHg). In the second experiment, food intake, and hence body weight, among the lesioned and sham-lesioned rats was equalized. Average MAP in the lesioned SHR at 7 and 15 wk postoperation was not different vs. sham-lesioned SHR but was significantly higher (191 +/- 6 mmHg) vs. sham-lesioned SHR but was significantly higher (191 +/- 6 mmHg) vs. sham-lesioned SHR (164 +/- 5 mmHg) 22 wk postoperation. These results indicate that destruction of neuronal perikarya in the ACe in young SHR merely delays the development of hypertension, due to a reduced weight gain.