Inflammation and Neurogenic Hypertension

Abstract

See related article, pages 263–270 The brain renin–angiotensin system (RAS) plays a critical role in maintaining blood pressure regulation and volume homeostasis. Components of the RAS, including angiotensinogen, renin, angiotensin (Ang)-converting enzymes, and Ang receptors, are expressed in various nuclei located between the anteroventral region of the third ventricle (AV3V) and the brain stem.1,2 Accordingly, formation of the various Ang peptides, notably Ang II and Ang(1-7) can take place in the brain, independently of the endocrine RAS, and participate in the regulation of water intake, salt appetite, cardiac baroreflex and autonomic functions. Upregulation of Ang II type 1 (AT1) receptors in these nuclei has been shown to reduce baroreflex sensitivity and increase sympathetic tone, thus contributing to the development and maintenance of hypertension and heart failure, ultimately leading to end-organ damage.3 On the other hand, treatment with ACE inhibitors and Ang receptor blockers can prevent RAS overactivity and restore a normal cardiovascular function. In addition to Ang II generated in the brain, blood-borne Ang peptides can also enter the central nervous system via the circumventricular organs (CVOs) and contribute to the regulation of blood pressure and volume homeostasis.4 The CVOs are represented by the OVLT (organum vasculosum of the lamina terminalis), the subfornical organ (SFO), the median eminence and the neurohypophysis, …