Martynowicz Helena, Janus Agnieszka, Nowacki Dorian, Mazur Grzegorz
Department and Clinic of Internal and Occupational Diseases and Hypertension, Wroclaw Medical University, Poland.
Adv Clin Exp Med. 2014 May-Jun;23(3):319-25. doi: 10.17219/acem/37123.
Hypertension is a major risk factor for cardiovascular disease, which is a serious health problem in the highly industrialized countries. In more than 95% of the cases, the etiology of hypertension remains unknown. A key role in the etiology of hypertension is played by endothelial dysfunction and the inflammatory reaction in the vascular wall, in which the low molecular weight proteins so called chemokines are involved. The chemokines involved in the pathogenesis of hypertension include monocyte chemoattractant protein-1, MCP-1, CCL2, interferon-inducible protein (IP-10; CXCL10), interleukin-8 (IL-8; CXCL8), RANTES (CCL5), fractalkine (CX3CL1) and their receptors CCR2, CCR5, CXCR1, CXCR2, CXCR3 and CX3CR1. The mechanisms involving chemokines and their receptors in the pathogenesis of hypertension are complex and not fully understood. They include the impact of the migration of macrophages and monocytes to the vascular wall, endothelial dysfunction, effects on nitric oxide and endothelin-1 and smooth muscle cell proliferation. Chemokines are also involved in the pathogenesis of complications of hypertension, such as atherosclerosis, myocardial and renal fibrosis. In Poland, only about 26% of patients are effectively treated with antihypertensive drugs. The use of new therapeutic methods based on the inhibition of the inflammatory process in the vascular wall, including the impact on the function of chemokines and their receptors, could improve the effectiveness of the treatment of hypertension.
高血压是心血管疾病的主要危险因素，而心血管疾病在高度工业化国家是一个严重的健康问题。在超过95%的病例中，高血压的病因仍然不明。血管内皮功能障碍和血管壁的炎症反应在高血压病因中起关键作用，其中涉及所谓的趋化因子这种低分子量蛋白质。参与高血压发病机制的趋化因子包括单核细胞趋化蛋白-1（MCP-1、CCL2）、干扰素诱导蛋白（IP-10；CXCL10）、白细胞介素-8（IL-8；CXCL8）、调节激活正常T细胞表达和分泌因子（RANTES；CCL5）、 fractalkine（CX3CL1）及其受体CCR2、CCR5、CXCR1、CXCR2、CXCR3和CX3CR1。趋化因子及其受体在高血压发病机制中的作用机制复杂，尚未完全了解。这些机制包括巨噬细胞和单核细胞向血管壁迁移的影响、内皮功能障碍、对一氧化氮和内皮素-1的影响以及平滑肌细胞增殖。趋化因子还参与高血压并发症的发病机制，如动脉粥样硬化、心肌和肾纤维化。在波兰，只有约26%的患者通过抗高血压药物得到有效治疗。基于抑制血管壁炎症过程的新治疗方法的应用，包括对趋化因子及其受体功能的影响，可能会提高高血压的治疗效果。
