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Two putative mechanisms are explored in this manuscript. First, brain mineralocorticoid receptors may influence sympathetic discharge by regulating the release of pro\u2010inflammatory cytokines into the circulation. Blood\u2010borne pro\u2010inflammatory cytokines act upon receptors in the microvasculature of the brain to induce cyclooxygenase\u20102 activity and the production of prostaglandin E<jats:sub>2<\/jats:sub>, which penetrates the blood\u2013brain barrier to activate the sympathetic nervous system. Second, brain mineralocorticoid receptors may influence sympathetic drive by upregulating the activity of the brain renin\u2013angiotensin system, resulting in NAD(P)H oxidase\u2010dependent superoxide production. A potential role for superoxide\u2010dependent mitogen\u2010activated protein kinase signalling pathways in the regulation of sympathetic nerve activity is also considered. Other potential downstream signalling mechanisms contributing to mineralocorticoid receptor\u2010mediated sympathetic excitation are under investigation.<\/jats:p>","DOI":"10.1113\/expphysiol.2008.045948","type":"journal-article","created":{"date-parts":[[2009,8,1]],"date-time":"2009-08-01T01:37:03Z","timestamp":1249090623000},"page":"19-25","source":"Crossref","is-referenced-by-count":69,"title":["Mineralocorticoid receptors, inflammation and sympathetic drive in a rat model of systolic heart failure"],"prefix":"10.1113","volume":"95","author":[{"given":"Robert 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