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Prolonged ouabain infusion induces hypertension in rodents, and ouabain\u2010resistant mutation of the \u03b12 ouabain binding site (\u03b12<jats:sup>R\/R<\/jats:sup>mice) confers resistance to several forms of hypertension. Pressure overload\u2010induced heart hypertrophy and failure are attenuated in cardio\u2010specific \u03b12 knockout, cardio\u2010specific \u03b12 overexpression and \u03b12<jats:sup>R\/R<\/jats:sup>mice. We propose a unifying hypothesis that reconciles these apparently disparate findings: brain mechanisms, activated by Ang\u00a0II and high NaCl, regulate sympathetic drive and a novel neurohumoral pathway mediated by both brain and circulating endogenous ouabain (EO). Circulating EO modulates ouabain\u2010sensitive \u03b12 Na<jats:sup>+<\/jats:sup>pump activity and Ca<jats:sup>2+<\/jats:sup>transporter expression and, via Na<jats:sup>+<\/jats:sup>\/Ca<jats:sup>2+<\/jats:sup>exchange, Ca<jats:sup>2+<\/jats:sup>homeostasis. 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