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J Inflamm (Lond). 2010 May 12;7:21. doi: 10.1186/1476-9255-7-21.

Captopril reduces cardiac inflammatory markers in spontaneously hypertensive rats by inactivation of NF-kB.

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Departamento de Fisiología y Zoología, Facultad de Farmacia, Universidad de Sevilla, E-41012 Sevilla, Spain.



Captopril is an angiotensin-converting enzyme (ACE) inhibitor widely used in the treatment of arterial hypertension and cardiovascular diseases. Our objective was to study whether captopril is able to attenuate the cardiac inflammatory process associated with arterial hypertension.


Left ventricle mRNA expression and plasma levels of pro-inflammatory (interleukin-1beta (IL-1beta) and IL-6) and anti-inflammatory (IL-10) cytokines, were measured in spontaneously hypertensive rats (SHR) and their control normotensive, Wistar-Kyoto (WKY) rats, with or without a 12-week treatment with captopril (80 mg/Kg/day; n = six animals per group). To understand the mechanisms involved in the effect of captopril, mRNA expression of ACE, angiotensin II type I receptor (AT1R) and p22phox (a subunit of NADPH oxidase), as well as NF-kappaB activation and expression, were measured in the left ventricle of these animals.


In SHR, the observed increases in blood pressures, heart rate, left ventricle relative weight, plasma levels and cardiac mRNA expression of IL-1beta and IL-6, as well as the reductions in the plasma levels and in the cardiac mRNA expression of IL-10, were reversed after the treatment with captopril. Moreover, the mRNA expressions of ACE, AT1R and p22phox, which were enhanced in the left ventricle of SHR, were reduced to normal values after captopril treatment. Finally, SHR presented an elevated cardiac mRNA expression and activation of the transcription nuclear factor, NF-kappaB, accompanied by a reduced expression of its inhibitor, IkappaB; captopril administration corrected the observed changes in all these parameters.


These findings show that captopril decreases the inflammation process in the left ventricle of hypertensive rats and suggest that NF-kappaB-driven inflammatory reactivity might be responsible for this effect through an inactivation of NF-kappaB-dependent pro-inflammatory factors.

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