CAJ | 학술논문

[目的]探讨柚皮素对大鼠离体肾动脉血管环的舒张作用及其机制。[方法]通过 DMT 微血管张力记录仪和Powerlab张力换能器记录其张力变化。将肾动脉血管环用氯化钾(60 mmol/L)或苯肾上腺素(10-5 mol/L)预收缩达平台后,用柚皮素(10-6 mol/L~10-4 mol/L)对肾动脉进行浓度依赖性的舒张,测定柚皮素对预收缩肾动脉的舒张百分比。观察柚皮素预孵(浓度选舒张实验中计算的 RC50值)前后60 mmol/L 氯化钾或10-5 mol/L苯肾上腺素收缩肾动脉幅度的变化。用氯化钾或苯肾上腺素预收缩肾动脉达平台后,孵育Kir通道抑制剂氯化钡(BaCl210-4 mol/L)、KCa通道抑制剂四乙胺(TEA,10-3 mol/L)15 min,达平台后,依次加入不同浓度的柚皮素(10-6 mol/L~10-4 mol/L)对其进行舒张,观察BaCl2、TEA对柚皮素舒张肾动脉作用的影响。[结果]柚皮素在10-6 mol/L~10-4 mol/L内对氯化钾或苯肾上腺素预收缩大鼠离体肾动脉血管环均具有浓度依赖性的舒张作用；提前孵育柚皮素,使氯化钾或苯肾上腺素收缩大鼠离体肾动脉血管环的幅度发生一定程度的降低,分别降低了(53.10±2.43)%、(46.39±3.24)%；Kir 通道抑制剂氯化钡(10-4 mol/L)对柚皮素舒张60 mmol/L 氯化钾或10-5 mol/L 苯肾上腺素预收缩肾动脉血管环的作用没有明显的影响,而 KCa通道抑制剂四乙胺对柚皮素舒张60 mmol/L氯化钾或10-5 mol/L 苯肾上腺素预收缩肾动脉的最大舒张幅度均有一定程度的抑制作用。[结论]柚皮素对高钾或苯肾上腺素预收缩的离体大鼠肾动脉血管环均有浓度依赖性的舒张效果；柚皮素对肾动脉血管环的舒张作用与钙激活钾通道KCa有关。
[목적]탐토유피소대대서리체신동맥혈관배적서장작용급기궤제。[방법]통과 DMT 미혈관장력기록의화Powerlab장력환능기기록기장력변화。장신동맥혈관배용록화갑(60 mmol/L)혹분신상선소(10-5 mol/L)예수축체평태후,용유피소(10-6 mol/L~10-4 mol/L)대신동맥진행농도의뢰성적서장,측정유피소대예수축신동맥적서장백분비。관찰유피소예부(농도선서장실험중계산적 RC50치)전후60 mmol/L 록화갑혹10-5 mol/L분신상선소수축신동맥폭도적변화。용록화갑혹분신상선소예수축신동맥체평태후,부육Kir통도억제제록화패(BaCl210-4 mol/L)、KCa통도억제제사을알(TEA,10-3 mol/L)15 min,체평태후,의차가입불동농도적유피소(10-6 mol/L~10-4 mol/L)대기진행서장,관찰BaCl2、TEA대유피소서장신동맥작용적영향。[결과]유피소재10-6 mol/L~10-4 mol/L내대록화갑혹분신상선소예수축대서리체신동맥혈관배균구유농도의뢰성적서장작용；제전부육유피소,사록화갑혹분신상선소수축대서리체신동맥혈관배적폭도발생일정정도적강저,분별강저료(53.10±2.43)%、(46.39±3.24)%；Kir 통도억제제록화패(10-4 mol/L)대유피소서장60 mmol/L 록화갑혹10-5 mol/L 분신상선소예수축신동맥혈관배적작용몰유명현적영향,이 KCa통도억제제사을알대유피소서장60 mmol/L록화갑혹10-5 mol/L 분신상선소예수축신동맥적최대서장폭도균유일정정도적억제작용。[결론]유피소대고갑혹분신상선소예수축적리체대서신동맥혈관배균유농도의뢰성적서장효과；유피소대신동맥혈관배적서장작용여개격활갑통도KCa유관。
Obj ective:To probe into the vasodilation effect of naringenin for rat renal artery rings and its mechanism.Methods:DMT capillary tension recorder and Powerlab tension transducer were used to record its changes of tension.The renal artery rings received pre contraction treatment with potassium chloride (60 mmol/L)or phenylephrine (10-5 mol/L)reached to the platform,and the concentration dependent vaso-dilation was implemented in the renal arteries by using naringenin (10-6 mol/L~10-4 mol/L),then to measure the vasodilation percentage of pre contracted renal artery.Before and after naringenin pre incubation (selected concentration was RC50 values calculated in diastole experi-ments )contraction amplitude changes of the renal arteries were ob-served after treatment with 60 mmol/L KCl or 10-5 mol/L phenyleph-rine.After potassium chloride or phenylephrine were used for pre con-striction of renal artery up to the platform,and incubation reached the platform with Kir channel inhibitor barium chloride (BaCl2 10-4 mol/L) and KCa channel inhibitor tetraethylammonium (TEA,10-3 mol/L)for 1 5 min,then in turn the different concentrations of naringenin (1 0-6 mol/L~1 0-4 mol/L)was added for relaxing the renal artery and then to observe the influence of BaCl2 and TEA on vasodilation of renal artery by naringenin.Results:Naringenin within 1 0-6 mol/L~1 0-4 mol/L had a concentration dependent vasodilation for KCl or phenylephrine pre constricted isolated rat renal artery rings;naringenin incubation in ad-vance can reduce contraction amplitude of rat kidney artery rings by KCl or phenylephrine to some extent,and it decreased by (53.10±2.43)%and (46.39±3.24)% respectively;Kir channel inhibitor barium chloride (1 0-4 mol/L)didn’t have significant influence on vasodilation effect of naringenin for 60 mmol/L KCl or 10-5 mol/L phenylephrine pre con-stricted renal artery rings,and KCa channel inhibitor tetraethylammoni-um (TEA,10-3 mol/L)had a certain degree of inhibition for maximum amplitude of vasodilation of naringenin for 60 mmol/L KCl or 10-5 mol/L phenylephrine pre constricted renal artery.Conclusion:Naringenin has the concentration dependent vasodilation effect for isolated renal arteri-al vascular rings in rats receiving potassium or phenylephrine pre con-stricted treatment;the vasodilation effect of naringenin on the renal ar-tery rings is related with calcium activated potassium channels KCa .