Despite tremendous research efforts, hypertension remains an epidemic health concern, leading often to the development of cardiovascular disease. It is well-established that in many instances, the brain plays an important role in the onset and progression of hypertension via activation of the sympathetic nervous system. Further, the activity of the renin angiotensin system (RAS) and of glial-mediated pro-inflammatory processes have independently been linked to this neural control and are, as a consequence, both attractive targets for the development of anti-hypertensive therapeutics. Although it is clear that the predominant effector peptide of the RAS, angiotensin-II, activates its type-1 receptor on neurons to mediate some of its hypertensive actions, additional nuances of this brain RAS control of blood pressure are constantly being uncovered. One of these complexities is that the RAS is now thought to impact cardiovascular control, in part, via facilitating a glial cell-dependent pro-inflammatory milieu within cardiovascular control centers. Another is that the newly-characterized antihypertensive limbs of the RAS are now recognized to, in many cases, antagonize the pro-hypertensive AT1R-mediated effects. That being said, the mechanism by which the RAS, glia and neurons interact to regulate blood pressure is an active area of ongoing research. Here we review the current understanding of these interactions and present a hypothetical model of how these exchanges may ultimately regulate cardiovascular function.
- blood pressure
- Copyright © 2015, American Journal of Physiology - Regulatory, Integrative and Comparative Physiology