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目的探讨花生四烯酸(AA)及5,6环氧二十碳三烯甘油酸(5,6EET)在肾近曲小管对血管紧张素Ⅱ(AngⅡ)刺激Na+和HCO3-重吸收的作用机制。方法手工分离野生鼠、cPLA2α缺陷鼠的单根肾近曲小管,分光光度法测定在AA或5,6EET作用下,低浓度(10-10mol/L)AngⅡ引起的Na+/HCO3-离子转运活动度变化,微灌注法测定HCO3-重吸收率的变化,Western blotting法测定不同情况下细胞外信号调节激酶(ERK)的磷酸化。结果在浓度10-7mol/LAA或10-7mol/L5,6EET作用下,浓度10-10mol/LAngⅡ刺激野生鼠和cPLA2α缺陷鼠在肾近曲小管Na+和HCO3-的重吸收作用被抑制,同时浓度10-10mol/LAngⅡ刺激ERK的磷酸化作用被抑制。结论在肾近曲小管cPLA2α/P450通路代谢产物AA及5,6EET通过抑制ERK磷酸化,阻止低浓度AngⅡ对Na+和HCO3-的重吸收。
Aim To investigate the mechanism of action of arachidonic acid (AA) and 5,6 epothilone (5,6EET) on renal tubular proximal tubule (Na +, HCO3-) reabsorption by angiotensin Ⅱ (AngⅡ) . Methods The single renal proximal tubule of wild mouse and cPLA2α-deficient mice was isolated by hand, and the activity of Na + / HCO3- induced by low concentration (10-10mol / L) AngⅡ was measured by spectrophotometry under the action of AA or 5,6EET The changes of HCO3-reabsorption were measured by microperfusion method. The phosphorylation of extracellular signal-regulated kinase (ERK) under different conditions was determined by Western blotting. Results Under the action of 10-7mol / LAA or 10-7mol / L 5,6EET, the reabsorption of Na + and HCO3- in the proximal tubules of wild-type mice and cPLA2α-deficient mice with 10-10mol / L of AngⅡ was inhibited, while the concentration The phosphorylation of ERK was inhibited by 10-10mol / LAngⅡ. Conclusions AA and 5,6EET, the metabolites of cPLA2α / P450 pathway in renal proximal tubule, prevent the reabsorption of Na + and HCO3- by low concentration of AngⅡ by inhibiting ERK phosphorylation.