The central nervous system plays a key role in the regulation of cardiovascular function, and alterations in the central neural mechanisms that control blood pressure may underlie the vast majority of cases of primary hypertension. The well-studied baroreceptor reflex powerfully regulates arterial pressure, though its involvement in the pathogenesis of chronic hypertension is likely to be only of minor importance. Supraspinal maintenance of sympathetic vasomotor outflow appears to emanate from neurons in the rostral ventrolateral medulla, and the tonic drive exerted on sympathetic vasomotor activity by the rostral ventrolateral medulla appears to be increased in several animal models of hypertension. In particular, the excitation of the rostral ventrolateral medulla by excitatory amino acid neurotransmitters and by stimulation of AT₁ angiotensin receptors appears to be increased in experimental hypertension. The current data support the view that neurogenic hypertension is mediated by increased excitatory drive of rostral ventrolateral medulla sympathoexcitatory neurons.