Key result
Long-term ACE inhibitors or AT1 antagonists reduce renal inflammation and proinflammatory factors in hypertensive rats.
Why the study?
Hypertension causes renal inflammation involving local angiotensin II production, prompting investigation into the role of AngII blockade in this inflammatory response.
Does long-term treatment with an ACE inhibitor or an AT1 antagonist reduce renal inflammation in spontaneously hypertensive rats with unilateral nephrectomy?
Does long-term treatment with an ACE inhibitor or an AT1 antagonist reduce renal inflammation in spontaneously hypertensive rats with unilateral nephrectomy?
Long-term ACE inhibition or AT1 blockade reduces renal inflammatory cell infiltration and proinflammatory factor up-regulation in a rat model of chronic hypertension with renal disease.
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 longterm 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 κB (NF-κB) and related genes. Both ACE inhibition and AT1 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 AT1 blockade or ACE inhibition can stop the renal inflammatory process in chronic hypertension-associated inflammatory response.
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Esteban et al. (2006) studied this question. Long-term ACE inhibitor or AT1 antagonist treatment reduced renal inflammatory cell infiltration and proinflammatory factor upregulation in hypertensive rats over 48 weeks.
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