Valsartan reduces interleukin-1beta secretion by peripheral blood mononuclear cells in patients with essential hypertension.

摘要

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-1beta (IL-1beta) secretion by peripheral blood mononuclear cells (PBMCs). In this study, we investigated whether treatment with valsartan, an angiotensin receptor blocker, lowered IL-1beta 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-1beta 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-1beta 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.