UNESP-UF: Hypertension Research Exchange Program

Resumo

This proposal centers on our ongoing collaborative projects on the anti-hypertensive actions of macrophage migration inhibitory factor (MIF) and angiotensin type 2 receptors (AT2R) that are mediated by the brain. Hypertension is a global health problem, and ~20 to 30% of hypertensive patients are resistant to available anti-hypertensive medications. It is generally accepted that the uncontrolled, resistant hypertension is primarily neurogenic in origin, involving over activity of the sympathetic nervous system and blunted baroreflexes that initiate and sustain high blood pressure. A major contributor to the changes in sympathetic activity and baroreflexes is the peptide angiotensin II (ANG II) acting via its neuronal type 1 receptors (AT1R) in cardiovascular control centers in the brainstem and hypothalamus. In addition, accumulating evidence accumulating evidence suggests that neuroinflammatory processes make a significant contribution to the sustained high blood pressure caused by over activity of ANG II. Indeed, the main proposal is to investigate the involvement and the role of MIF and AT2R in cardiovascular control centers in the hindbrain and hypothalamus in different experimental hypertension models. (AU)