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