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B/IB SYSTEM
1 Department of Physiology, School of Medicine, Universidad Complutense, Madrid, Spain
2 Medical Department, AstraZeneca Farmaceutica Spain, S.A, Madrid, Spain
* To whom correspondence should be addressed. E-mail: vcara{at}med.ucm.es.
We investigated the role of angiotensin II in vascular and circulating inflammatory markers in spontaneously hypertensive rats (SHR). To this end, aortic mRNA expression of IL-1
, IL-6 and TNF-
, as well as plasma levels of IL-1, IL-6 and TNF- were measured in adult SHR untreated or treated with either the AT1 receptor antagonist, candesartan (2 mg/Kg/d), or antihypertensive triple therapy (TT: hydralazine + hydrochlorothiazide + reserpine;20 + 7 + 0.15 mg/kg/d) for 10 weeks. Likewise, the aortic expression of NF
B p50 subunit precursor, p105, and its inhibitor (IB) were measured. Wistar Kyoto rats of the same age were used as a normotensive reference group. High blood pressure levels were associated with an increase (p<0.05) in aortic mRNA expression of IL-1, IL-6 and TNF-. Hypertension was also accompanied by an increase in plasma levels of both IL-1 and IL-6. No differences were observed in circulating levels of TNF- between SHR and WKY. SHR presented elevated aortic mRNA expression of the transcription factor NFB, and a reduction in its inhibitor IB. Candesartan decreased (p<0.05) blood pressure levels, aortic mRNA expression of IL-1, IL-6 and TNF- and (p<0.05) plasma concentration of IL-1 and IL-6. However, although arterial pressure decrease was comparable for both treatments, TT only partially reduced the increments in inflammatory markers. In fact, candesartan-treated rats showed significantly lower levels of both circulating and vascular inflammatory markers than animals receiving TT. Both treatments were able to increase IB mRNA expression in a similar manner. However, only candesartan reduced NFB mRNA expression. In summary, the results show that: 1) SHR presented a vascular inflammatory process; 2) angiotensin II, as well as an increase in hemodynamic forces associated with hypertension, seems to be involved in the stimulation of inflammatory mediators through the activation of NFB system; 3) the reduction of inflammatory mediators produced by candesartan in SHR could be partially due to both a down regulation of NFB and up regulation of IB.
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