Systemic Infusion of Angiotensin II into Normal Rats Activates Nuclear Factor-κB and AP-1 in the Kidney : Role of AT1 and AT2 Receptors

摘要: Recent studies have pointed out the implication of angiotensin II (Ang II) in various pathological settings. However, molecular mechanisms and AngII receptor (AT) subtypes involved are not fully identified. We investigated whether elicited vivo activation nuclear transcription factors that play important roles pathogenesis renal vascular injury. Systemic infusion Ang into normal rats increased factor (NF)-κB AP-1 binding activity was associated with inflammatory cell infiltration tubular damage. Interestingly, infiltrating cells presented activated NF-κB complexes, suggesting involvement activation. When were treated AT1 or AT2 antagonists different responses observed. The antagonist diminished glomerular abolished cells, improved damage normalized arterial blood pressure. mononuclear without any effect on These data suggest mainly mediates injury via AP-1/NF-κB, whereas participates kidney by NF-κB. Our results provide novel information signaling support recent view as a proinflammatory modulator.