Brain angiotensin peptides regulate sympathetic tone and blood pressure

Brain angiotensin II (Ang II) induces tonic sympathoexcitatory effects through AT(1) receptor stimulation of glutamatergic neurons and sympathoinhibitory effects via GABAergic neurons in the rostral ventrolateral medulla, the brainstem 'pressor area'. NADPH-derived superoxide production and reactive oxygen species signalling is critical in these actions, and AT(2) receptors in the rostral ventrolateral medulla appear to mediate opposing effects on sympathetic outflow. In the hypothalamic paraventricular nucleus, Ang II has AT(1) receptor-mediated sympathoexcitatory effects and enhances nitric oxide formation, which in turn inhibits the Ang II effects through a GABAergic mechanism. Ang II also decreases the tonic sympathoinhibitory effect of gamma amino butyric acid within the paraventricular nucleus. Angiotensin III and Angiotensin IV increase blood pressure via brain AT(1) receptor stimulation. Angiotensin (1-7) influences cardiovascular function through a specific Mas-receptor. This review examines the evidence that brain angiotensin peptides, glutamate, gamma amino butyric acid and nitric oxide interact within the rostral ventrolateral medulla and paraventricular nucleus to control sympathetic tone and blood pressure. J Hypertens 28: 1599-1610 (c) 2010 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.