肥胖贡献了65-75%的人初级(必需)高血压风险,这是心血管和肾脏疾病的主要司机。肾功能紊乱,与肾脏钠重吸收和补偿性肾小球高滤育增加相关,在启动肥胖高血压和靶器官损伤方面发挥着关键作用。肾功能紊乱和血压增加的介质包括1)肾交感神经活动(RSNA)升高;2)增加血管紧张素II和醛固酮如血管紧张素II和醛固酮;3)Natriuric激素的相对缺乏;4)肾脏脂肪肾上压缩,肾脏周围;5)活化在整个身体中侵入组织的先天和适应性免疫细胞,产生有助于血管和靶器官损伤的炎性细胞因子/趋化因子,加剧高血压。这些神经异常,肾病和肥胖高血压的炎症机制是相互依赖的。例如,过量的肥胖增加了通过刺激中枢神经系统ProOpioMelanocortin-Melanocortin 4受体途径来增加RSNA的脂肪细胞衍生的细胞因子瘦蛋白。虽然肥胖也可以使肥胖也可能与醛固酮相似,伴随着肾小序素 - 醛固酮系统活化的过量的内脏,前升和肾鼻窦脂肪压缩肾脏。 Prolonged obesity, hypertension, metabolic abnormalities, and inflammation cause progressive renal injury, making hypertension more resistant to therapy and often requiring multiple antihypertensive drugs and concurrent treatment of dyslipidemia, insulin resistance, diabetes, and inflammation. More effective anti-obesity drugs are needed to prevent the cascade of cardiorenal, metabolic, and immune disorders that threaten to overwhelm health care systems as obesity prevalence continues to increase.
代表欧洲心脏病学会发表。版权所有。©作者2020.对于权限,请发送电子邮件:Journals.permissions@oup.com。

参考

PubMed.