The medial amygdaloid area is involved in activation of angiotensin II-sensitive neurons in the anterior hypothalamic area.

We have previously reported that some neurons in the anterior hypothalamic area (AHA) are tonically activated by endogenous angiotensins in rats and that the activities of these AHA angiotensin II-sensitive neurons are enhanced in spontaneously hypertensive rats. It is suggested that there exist neural projections from the medial amygdala to the AHA in rats. In this study, we examined whether neurons in the medial amygdaloid area (MeA) are involved in the activation of AHA angiotensin II-sensitive neurons.

Contribution of the medial amygdaloid nucleus to the development of hypertension in spontaneously hypertensive rats.

We previously demonstrated involvement of the medial amygdaloid nucleus in restraint stress-induced pressor responses in rats. In this study, neuronal perikarya in the medial amygdaloid nucleus of 4-week-old spontaneously hypertensive rats (SHR) were selectively destroyed with ibotenic acid. Bilateral lesions of the medial amygdaloid nucleus attenuated the development of hypertension in SHR.

Involvement of the medial amygdaloid nucleus in restraint stress-induced pressor responses in rats.

Restraint stress increased the number of neurons with Fos immunoreactivity in the medial amygdaloid nucleus in rats and caused an increase in blood pressure. The stress-induced pressor response was inhibited by muscimol (80 pmol), a neuroinhibitory compound, injected bilaterally into the medial amygdaloid area, whereas muscimol (8 pmol) similarly injected had only a tendency of inhibition of the pressor response. These data suggest that the medial amygdaloid nucleus is involved in mediation of the restraint stress-induced pressor response.