The mechanisms by which dietary salt promotes hypertension are unknown. Previous work established that plasma [Na+] and osmolality rise in proportion with saltintake and thus promote release of vasopressin (VP) from the neurohypophysis. Although high levels of circulating VP can increase bloodpressure, this effect is normally prevented by a potent GABAergic inhibition of VP neurons by aortic baroreceptors. Here we show that chronic highsaltintake impairs baroreceptor inhibition of rat VP neurons through a brain-derived neurotrophic factor (BDNF)-dependent activation of TrkB receptors and downregulation of KCC2 expression, which prevents inhibitory GABAergic signaling. We show that highsaltintakeincreases the spontaneous firing rate of VP neurons in vivo and that circulating VP contributes significantly to the elevation of arterial pressure under these conditions. These results provide the first demonstration that dietary salt can affect bloodpressure through neurotrophin-induced plasticity in a central homeostatic circuit.
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