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.
Esteban
Vanesa
V
Laboratory of Cellular Biology in Renal Diseases, Universidad Autonoma, Madrid, Spain.
Gallego-Delgado
Julio
J
Lazaro
Alberto
A
Osende
Julio
J
Mezzano
Sergio
S
Egido
Jesus
J
Ruiz-Ortega
Marta
M
D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D006973:Hypertension / Q000150:complications / Q000378:metabolism; D018836:Inflammation Mediators / Q000378:metabolism; D019808:Losartan / Q000494:pharmacology*; D009393:Nephritis / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D000077583:Quinapril; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D044005:Tetrahydroisoquinolines / Q000494:pharmacology*; D013997:Time Factors; D015854:Up-Regulation / Q000187:drug effects
D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D018836:Inflammation Mediators; D044005:Tetrahydroisoquinolines; D019808:Losartan; D000077583:Quinapril