Li Quan-Zhong, Deng Qin, Li Jie-Qi, Yi Guang-Hui, Zhao Shui-Ping
Department of Cardiology, The Affiliated Hospital of Guilin Medical College, 15# Lequn Road, Guilin, Guangxi 541001, PR China.
Clin Chim Acta. 2005 May;355(1-2):131-6. doi: 10.1016/j.cccn.2004.12.006.
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.
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).
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).
We suggest a direct anti-inflammatory effect of valsartan and a pro-inflammatory effect of Ang II in patients with essential hypertension.
慢性低度炎症反应可能参与原发性高血压的病理过程。血管紧张素II（Ang II）可能部分参与了这一过程。我们早期的研究表明，原发性高血压患者外周血单核细胞（PBMCs）分泌的白细胞介素-1β（IL-1β）增加。在本研究中，我们调查了血管紧张素受体阻滞剂缬沙坦治疗是否能降低原发性高血压患者PBMCs分泌IL-1β。
24例原发性高血压患者被随机分为缬沙坦治疗组（80mg/天，B组）或匹配的常规治疗组（A组），治疗2周。通过梯度离心分离PBMCs。采用酶联免疫吸附测定（ELISA）法检测PBMCs上清液中IL-1β浓度。
与常规治疗组相比，缬沙坦治疗的患者在脂多糖刺激后PBMCs中IL-1β分泌减少（2857±643 vs. 2146±508 pg/ml，P<0.05）。
我们认为缬沙坦对原发性高血压患者有直接抗炎作用，而Ang II有促炎作用。
