饮食钾缓解盐诱导的冠状动脉损伤*

 目的：探讨饮食钾对盐诱导的冠状动脉损伤的保护机制。方法: 将4周龄SD大鼠随机分为3组，每组10只，分别是对照组（NS，蒸馏水）、高盐组（HS，含1.5% NaCl蒸馏水）和高盐补钾组（HS+HP，含1.5% NaCl和0.5% KCl蒸馏水）干预16周。每2周监测各组大鼠尾动脉血压。干预16周后，硝酸还原酶法检测大鼠血清中NO的含量；硫代巴比妥酸法检测各组大鼠血清中丙二醛（MDA）的含量; HE染色观察各组大鼠左冠状动脉的大体形态；免疫荧光染色观察各组大鼠冠状动脉内皮型一氧化氮合酶（eNOS）的表达；二氢乙啶荧光探针染色/Western blotting法观察各组大鼠冠状动脉氧化应激的程度。结果：高盐干预16周后，高盐组大鼠根据尾动脉血压的变化分为盐敏感性大鼠和盐抵抗性大鼠。本实验只研究HS组中盐敏感性大鼠。在HS组中，大鼠血压较NS组显著升高，给予补钾后可以缓解血压的升高。HS组较NS组大鼠血清中NO降低，MDA升高，冠状动脉eNOS表达降低,还原型烟酰胺腺嘌呤二核苷酸磷酸（NADPH）氧化酶的gp91亚基表达升高，冠状动脉管壁厚度显著增加，且 DHE荧光探针染色发现其超氧阴离子增加。高盐摄入的同时给予补钾可以缓解高盐摄入引起的有害效应。结论：高盐摄入通过氧化应激引起冠状动脉结构和功能的改变，补钾可以缓解这一效应的发生。

Potassium antagonizes damage of coronary artery induced by high salt intake

AIM：To investigate the effect of potassium treatment on coronary arterial impairment induced by high salt intake. METHODS：Sprague-Dawley rats (4-week-old, n=10 in each group) received distilled water (NS), water containing 1.5% NaCl (HS), or 1.5% NaCl and 0.5% KCl (HS+HP) for 16 weeks. Systolic blood pressure (SBP) was determined by tail plethysmography every 2 weeks. After 16 weeks of treatment, vascular remodeling, superoxide production， malondialdehyde (MDA) content, and endothelial nitric oxide synthase (eNOS) and gp91 expression in the coronary arteries were detected. RESULTS：After 16 weeks of salt loading, the rats in HS group was divided into salt sensitive subgroup and salt resistance subgroup according to the tail-cuff blood pressure. In this experiment, the salt-sensitive rats were selected as HS group. In HS group, salt loading significantly increased SBP, serum MDA and gp91 expression, decreased serum NO and eNOS expression in the coronary arteries, and induced the coronary artery remodeling compared with NS group. In salt-loaded SD rats, 16-week potassium treatment abrogated the effects induced by salt loading. CONCLUSION：High salt may affect structural and functional changes in coronary arteries by activating oxidative stress. Potassium treatment antagonizes the effect of high salt intake.