Abstract

Background Chronic low-grade inflammation response may contribute to the pathology of essential hypertension. Angiotensin II (Ang II) may be partly responsible for this process. Our early studies showed that individuals with essential hypertension had increased interleukin-1β (IL-1β) secretion by peripheral blood mononuclear cells (PBMCs). In this study, we investigated whether treatment with valsartan, an angiotensin receptor blocker, lowered IL-1β secretion by PBMCs in patients with essential hypertension. Methods Twenty-four patients with essential hypertension were randomized to treatment with valsartan (80 mg/day, group B) or matching routine therapy group (group A) for 2 weeks. PBMCs were isolated by gradient centrifugation. IL-1β concentrations in supernatant from PBMCs were measured by enzyme-linked immunosorbent assay (ELISA). Results Compared with routine therapy group, patients treated with valsartan had decreased secretion of IL-1β in PBMCs after stimulated by lipopolysaccharide (2857±643 vs. 2146±508 pg/ml, P<0.05). Conclusions We suggest a direct anti-inflammatory effect of valsartan and a pro-inflammatory effect of Ang II in patients with essential hypertension.

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