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This Article Full Text Full Text (PDF) All Versions of this Article: 92/3/471    most recent expphysiol.2006.036830v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Mayorov, D. N. Search for Related Content PubMed PubMed Citation Articles by Mayorov, D. N. Related Collections Review Articles Cardiovascular control

¹ Baker Heart Research Institute, Melbourne, Victoria, Australia

Cardiovascular reactivity, an abrupt increase in blood pressure and heart rate in response to emotional stress, is a risk factor for hypertension and heart disease. Brain angiotensin II (Ang II) type 1 (AT₁) receptor is increasingly recognized as an important regulator of cardiovascular reactivity. Given that a wide variety of AT₁ receptor signalling pathways exists in neurones, the precise molecular mechanisms that underlie central cardiovascular actions of Ang II during emotional stress are yet to be determined. Growing evidence, however, indicates that reactive oxygen species, and in particular superoxide (·O₂^–), are important intracellular messengers of many actions of brain Ang II. In particular, studies employing microinjection of ·O₂^– scavengers directly into the rostral ventrolateral medulla (RVLM) and dorsomedial hypothalamus of rabbits have shown that the activation of AT₁ receptor–·O₂^– signalling is required for full manifestation of the cardiovascular response to emotional stress. This role of ·O₂^– appears to be highly specific, because ·O₂^– scavengers in the RVLM do not alter the sympathoexcitatory response to baroreceptor unloading or sciatic nerve stimulation. The subcellular mechanisms for the stress-induced ·O₂^– production are likely to include the activation of NADPH oxidase and are essentially independent of nitric oxide. This review summarizes current knowledge of redox-sensitive signalling mechanisms in the brain that regulate cardiovascular effects of stress. Additionally, it presents initial evidence that ·O₂^– may be less important in the activation of central pressor pathways mediating cardiovascular arousal associated with appetitive events, such as food anticipation and feeding.

(Received 20 December 2006; accepted after revision 14 February 2007; first published online 15 February 2007)
Corresponding author D. N. Mayorov: Baker Heart Research Institute, PO Box 6492, St Kilda Road Central, Melbourne, Victoria 8008, Australia. Email: dmitry.mayorov{at}baker.edu.au