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This editorial refers to ‘ACE2 overexpression in the paraventricular nucleus attenuates angiotensin II-induced hypertension’ by S. Sriramula et al ., pp. 401–408, this issue. Angiotensin II increases arterial pressure through its multiple actions on the nervous system, the adrenal glands, the vasculature, and renal epithelial transport. In recent years, evidence has accumulated that the activation of proinflammatory mechanisms contributes to the pathogenesis of arterial hypertension by causing inflammation of tissues and organs, such as the vasculature, the kidneys, and the central nervous system (CNS).1 Angiotensin II is a potent stimulator of proinflammatory activity in hypertension.1,2The paraventricular nucleus (PVN) of the hypothalamus is intimately involved in neuroendocrine regulatory processes that affect arterial pressure.3 It receives inputs from osmosensitive neurons, arterial baroreceptors, and stretch receptors in the large veins and in the atria.3,4 The PVN effector neurons project to the posterior pituitary where they release oxytocin or vasopressin and to the anterior pituitary where they secrete releasing hormones into the portal circulation. Other neurons of the PVN project to CNS target neurons outside the pituitary that determine sympathetic and parasympathetic output.3,5 Stimulation of PVN neurons by circulating angiotensin II increases vasopressin release, elevates sympathetic activity, …

Antihypertensive effects of ACE2 in the paraventricular nucleus: a consequence of reduced neuroinflammation?