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See related article, pages 772–780 The central regulation of sympathetic nerve activity has been extensively investigated in normal and disease states since the detailed description of the cardiovascular pressor area by Alexander in 1946.1 This so called “pressor area” we now know to be the rostral ventrolateral medulla (RVLM). The neurons of the RVLM constitute the primary motor neuron pool from which sympathetic projections to the spinal cord arise. Importantly, the RVLM also receives inputs from a variety of integrative areas in the hypothalamus and medulla. The net sympathetic outflow of various cardiovascular reflexogenic areas have a common pathway which exits the brain from the RVLM. In addition to the neural modulation of these reflexes from hard wired areas in the hypothalamus, medulla, and forebrain, it has become increasingly more recognized that autocrine, paracrine, and endocrine influences on these sympathetic neurons are important for the regulation of arterial pressure, myocardial function, salt and water balance, and general cardiovascular homeostasis in the normal resting state and during the extremes of cardiovascular function such as exercise, heart failure, hypertension, etc.2–5Neuronal excitability in the RVLM is not only modulated by classical neurotransmitters such as glutamate and gamma amino butyric acid (GABA) but appears also to be regulated by the ubiquitous octapeptide angiotensin II (Ang II).6–8 In fact, Ang II, in addition to its myriad of cardiovascular and endocrine effects, has been known for many years to modulate sympathetic function …

The Regulation of Sympathetic Nerve Activity by Angiotensin II Involves Reactive Oxygen Species and MAPK