Direct hypothalamo-autonomic connections

Abstract

Angiotensin II (AngII), both circulating and centrally produced, acts as a neurotransmitter in the central autonomic pathway influencing the excitability of central nervous system neurons and subsequently influencing cardiovascular regulation. Accordingly, Ang II receptors have been widely characterized centrally, including within cardiovascular nuclei, such as the paraventricular nucleus, rostral ventrolateral medulla, and nucleus of tracts solitarius, which directly influence baroreflex control and sympathetic activity. Dysregulation of Ang II signaling in those autonomic pathways is associated with increased sympathetic activity and is considered a hallmark of hypertension in humans and experimental models. This chapter aims to highlight some of the underlying mechanisms by which Ang II promotes neuroinflammation with a consequent increase in sympathetic outflow in cardiovascular nuclei. We discuss the critical role of Ang II in blood–brain barrier permeability, the cross-talk of Ang II with the innate immune system response, and Ang II effects in the bradykinin system—all mechanisms leading to neuroinflammation.