The contribution of sympathetic activation in the development of hypertension is supported by early experimental evidence based on surgical denervation of sino-aortic baroreceptors or lesions of the central relay station of the baroreflex, the nucleus tractus solitarii. Disruption of this area of the brain was associated with an immediate increase in blood pressure. Sympathetic overactivity can also be triggered by impairment of the inhibitory function physiologically exerted by reflexogenic areas (arterial baroreceptors, cardiopulmonary receptors, and chemoreceptors) on adrenergic drive. Metabolic and humoral mechanisms are also thought to be involved in the development and progression of hypertension-related sympathetic overdrive.