Long-term treatment with an ACE inhibitor or an AT1 antagonist avoids hypertension-induced inflammation in the kidney.

Background: Hypertension causes an inflammatory response in the kidney. Many studies have demonstrated that activation of the renal renin-angiotensin system, and therefore an increase in local angiotensin II (AngII) production, participates in the renal inflammatory cell recruitment. Our aim was to investigate the role of AngII blockade in hypertension-induced inflammatory response.
Methods: To replicate chronic hypertension with renal disease, we used a model of spontaneously hypertensive rats with unilateral nephrectomy (UNX-SHR). These animals were studied for 48 weeks. We investigated the effect of long-term treatment with an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin II type 1 (AT1 ) antagonist, 2 strategies currently used in humans, on renal proinflammatory parameters.
Results: UNX-SHR rats presented elevated renal inflammatory cell infiltration and up-regulation of proinflammatory factors, including activation of nuclear factor chi B (NF-chi B) and related genes. Both ACE inhibition and AT 1 blockade decreased the number of inflammatory cells as well as the up-regulation of proinflammatory factors in the kidney.
Conclusions: These results suggest that either AT 1 blockade or ACE inhibition can stop the renal inflammatory process in chronic hypertension-associated inflammatory response.