R epeated exposure to stress may favor, both in experimental animals and in humans, an increase in blood pressure, leading in some instances to a true hypertensive state. It is thought that stress-induced hypertension is mediated by sympathetic nervous system activation that in turn, by exerting vasoconstrictor effects and increasing heart rate (and thus cardiac output), may promote the development and progression of the hypertensive state. A new study by Beetz and colleagues in this issue of the JCI, which reports the results of experimental studies carried out in both mice and humans, reveals the potential role of the phosducin gene in modulating the adrenergic and blood pressure responses to stress (see the related article beginning on page 3597).