Abstract

See related article, pp 564–571 Gomez-Sanchez et al1 published 2 crucial articles in 2005.1,2 One established that aldosterone could be synthesized in vivo in the rat brain.1 The other demonstrated that intracerebroventricular infusion of trilostane, to inhibit of aldosterone and corticosterone synthesis in the brains of Dahl salt-sensitive rats, reversed salt-induced hypertension. These carefully performed studies raised the possibility that in addition to circulating aldosterone, aldosterone synthesized locally in the brain could play a physiological role in the regulation of blood pressure. Subsequently, Huang et al3 and Gomez-Sanchez et al4 used a more selective inhibitor of aldosterone synthase, FAD286,5 and reported attenuation or reversal of salt-sensitive hypertension in Dahl salt-sensitive rats. Those articles provided additional support for the hypothesis that salt-induced hypertension in Dahl salt-sensitive rats is, in part, dependent on elevated expression of aldosterone synthase within the brain, resulting in increased local production of aldosterone. Was the physiological relevance of locally produced aldosterone unique to this genetic model of hypertension? In this issue of Hypertension , the article by Huang et al6 shows that intracerebroventricular infusion of either …

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