Hypertension is associated with autonomic nervous system dysfunction. Elevated sympathetic outflow and alterations in the baroreceptor reflex sensitivity may play an important role in the initiation and maintenance of high blood pressure. Previous work from this laboratory has demonstrated that endothelial derived genes are differentially expressed in key brainstem nuclei in hypertensive rats. In addition, angiotensin II acting at the nucleus tractus solitarii has been shown to attenuate the baroreflex through a vascular-neuronal signalling mechanism involving the release of nitric oxide. This evidence has led to the hypothesis that alterations in brainstem microvascular gene expression are causative to hypertension in animals and man.