Editorial Focus: The Brain Renin-Angiotensin System and Hypertension Focus on: Hypertension in mice with transgenic activation of the brain renin-angiotensin system is vasopressin dependent

The brain renin-angiotensin system (RAS) has been extensively studied due to its role in central cardiovascular regulation and body fluid homeostasis. Much of the early work on this system was stimulated by the pioneering work of Brody, Johnson, and colleagues who focused on possible interactions between circulating angiotensin II and a brain RAS promoting neurogenic hypertension (1). Our current understanding of the brain RAS has evolved to include multiple neuroactive peptides that have differential effects in regulating of the autonomic nervous system not only in the context of hypertension but also in congestive heart failure, fetal programed cardiovascular disease and aging (2, 4, 7, 8). Many of the advances in our understanding of the complexity of this system have been the result of new transgenic approaches that permit tissue specific expression or deletion of important components of RAS. In the recent publication by Littlejohn et al. (5), a sophisticated double transgenic mouse model was used to examine the effects of selective activation of the brain RAS system on blood pressure and water and electrolyte homeostasis. In this model, the brain is selectively targeted by combining two separate mouse models: one with selective overexpression of human renin driven by the neuron specific promoter, synapsin, and another with human angiotensinoge