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Brain mechanisms are involved in the pathogenesis of hypertension.Pro-inflammatory cytokines (PIC) and their nuclear transcription factor (NF-κB) are activated in the neurons of hypothalamic paraventricular nucleus (PVN), thereby contributing to the pathophysiology of hypertension.However, the role played by microglia in the PVN is not known.The present study was undertaken to confirm that activated microglial cells produce PIC and induce oxidative stress and contribute to the progression of hypertension.Methods:Rats were infused intravenously with angiotensin Ⅱ (ANGⅡ, 0.6μg/hr) or saline for 4 weeks,while one group received pyrrolidine dithiocarbamate (PDTC, 5 μg/hr), an inhibitor of NF-κB,via bilateral PVN cannula along with ANGⅡ (iv).In ANG Ⅱ+vehicle rats, mean blood pressure (MAP) was increased on day 4 and remained elevated throughout the study.ANGⅡ infused animals hadmore activated microglia in the PVN, with increased expression of PIC,gp9 lphox, and COX-2staining in the PVN when compared with saline-infused rats.ANGⅡ infused animals also had increased levels of PGE2 in the CSF and PIC in the plasma.ANGⅡ infused rats had increased renal sympathetic activity (RSNA) accompanied by increased plasma norepinphrine levels.Treatment with PDTC resulted in fewer activated microglia,with decreased expression of PIC, gp91phox and COX-2 in the PVN.Treatment with PDTC also decreased plasma concentrations of PIC and NE.These findings suggest that activated microglial cells increase PIC in the PVN and contribute to oxidative stress in ANGⅡ-infused hypertensive rats.This increased superoxide and activated NF-κB contribute to the progression of hypertension.