CAJ | 학술논문

目的：通过研究原发性高血压患者WNK1激酶( with no lysine kinase 1)-STE20相关脯氨酸/丙氨酸丰富激酶( Ste20-related proline/alanine-rich kinase,SPAK)信号通路的表达水平,以及低钠高钾饮食干预后表达水平的变化,探讨其在原发性高血压中的致病作用。方法：75名未经治疗的高血压患者经低钠高钾饮食干预1个月,通过Realtime PCR对干预前后外周血中的WNK1和SPAK的mRNA表达水平进行检测,并观察受试者血压、血尿生化指标变化。结果：高血压患者组外周血中WNK1和SPAK mRNA水平的表达较健康志愿者组明显升高,低钠高钾饮食干预后信号通路的表达则较基线期明显下降。统计学分析表明WNK1激酶的表达水平与血压之间存在相关性。结论：WNK1-SPAK激酶通路的表达异常可能参与原发性高血压的发病,饮食结构的变化可通过改变WNK1-SPAK-NCC信号通路的表达而调节血压。
목적：통과연구원발성고혈압환자WNK1격매( with no lysine kinase 1)-STE20상관포안산/병안산봉부격매( Ste20-related proline/alanine-rich kinase,SPAK)신호통로적표체수평,이급저납고갑음식간예후표체수평적변화,탐토기재원발성고혈압중적치병작용。방법：75명미경치료적고혈압환자경저납고갑음식간예1개월,통과Realtime PCR대간예전후외주혈중적WNK1화SPAK적mRNA표체수평진행검측,병관찰수시자혈압、혈뇨생화지표변화。결과：고혈압환자조외주혈중WNK1화SPAK mRNA수평적표체교건강지원자조명현승고,저납고갑음식간예후신호통로적표체칙교기선기명현하강。통계학분석표명WNK1격매적표체수평여혈압지간존재상관성。결론：WNK1-SPAK격매통로적표체이상가능삼여원발성고혈압적발병,음식결구적변화가통과개변WNK1-SPAK-NCC신호통로적표체이조절혈압。
Objective:To explore the pathogenic role of the WNK1(with no lysine kinase 1) -SPAK(Ste20-related pro-line/alanine-rich kinase) kinase signaling pathway in essential hypertension. We will investigate the expression of these kinases in essential hypertension patients before and after low sodium /high potassium diet transition. Methods:We detected the WNK1 and SPAK mRNA expression levels in the peripheral blood of 75 untreated hypertensive volunteers by Realtime PCR. And then we ob-served the changes in WNK1-SPAK cascade after low sodium and high potassium diet intervention for a month. Blood pressure,blood and urinary electrolytes were measured. Results:WNK1 and SPAK mRNA abundance in peripheral blood in hypertensive patients were increased significantly compared with healthy volunteers. The abundance of these kinases was significantly decreased after consuming low sodium /high potassium diet. Statistical analysis showed blood pressure was correlated with WNK1 kinase abundance. Conclusion:The expression of WNK1 and SPAK kinases pathway may be involved in the pathogenesis of essential hypertension. Low sodium high potassium diet may regulate blood pressure through inactivating WNK1-SPAK-NCC signaling pathway.