肥胖相关高血压中介导肾交感神经激活的机制。
Mechanisms mediating renal sympathetic nerve activation in obesity-related hypertension.
作者信息
Chen W, Leo S, Weng C, Yang X, Wu Y, Tang X
机构信息
Department of Cardiology, The Third Xiangya Hospital, Central South University, 410013, Changsha, China.
出版信息
Herz. 2015 Apr;40 Suppl 2:190-6. doi: 10.1007/s00059-014-4072-7.
Excessive renal sympathetic nerve activation may be one of the mechanisms underlying obesity-related hypertension. Impaired baroreflex sensitivity, adipokine disorders-such as leptin, adiponectin, and resistin-activation of the renin-angiotensin system, hyperinsulinemia, insulin resistance, and renal sodium retention present in obesity increase renal sympathetic nerve activity, thus contributing to the development of hypertension. Renal sympathetic denervation reduces both renal sympathetic activity and blood pressure in patients with obesity-related hypertension.
肾交感神经的过度激活可能是肥胖相关高血压的潜在机制之一。压力反射敏感性受损、脂肪因子紊乱（如瘦素、脂联素和抵抗素）、肾素-血管紧张素系统激活、高胰岛素血症、胰岛素抵抗以及肥胖时出现的肾钠潴留都会增加肾交感神经活性，从而导致高血压的发生。肾交感神经去神经支配可降低肥胖相关高血压患者的肾交感神经活性和血压。
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