Hypertension is the single most important risk factor for cardiovascular disease and, thus, remains a global public health challenge. Significant progress has been made during the last several decades in the treatment of hypertension through the use of inhibitors of the renin-angiotensin (Ang) system, with either Ang-converting enzyme inhibitors or Ang receptor type 1 blockers, diuretics, α-adrenoreceptor antagonists, and calcium channel blockers. Despite these advances, it has been extremely difficult to manage hypertension in 40% of hypertensive patients. 1 A majority of these unresponsive patients exhibit increased sympathetic drive and display neurogenic components. 2–4 The role of elevated sympathetic nervous system in drug-resistant hypertension is corroborated by the recent successes in its treatment by renal sympathetic denervation in humans. 3, 5, 6 These observations have led to the realization that elucidation and understanding of cellular, molecular, and physiological mechanisms involved in the development and establishment of neurogenic hypertension are pivotal in advancing new therapeutic strategies that would be effective in a majority of patients. The objectives of this article are to summarize recent advances in this field, underscoring the importance of coordinated neuralperipheral signaling in neural control of blood pressure (BP) and contribution of inflammatory molecules, and to introduce novel and emerging concepts in the pathogenesis of neurogenic hypertension. It is advised to consult other reviewers for details on fundamental studies related to neural pathways, the renin-Ang system, and involvement of other hormonal systems in neurogenic hypertension. 7–13