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首页> 外文期刊>American Journal of Physiology >Regulation of fluid reabsorption in rat or mouse proximal renal tubules by asymmetric dimethylarginine and dimethylarginine dimethylaminohydrolase 1
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Regulation of fluid reabsorption in rat or mouse proximal renal tubules by asymmetric dimethylarginine and dimethylarginine dimethylaminohydrolase 1

机译：通过不对称二甲基碱和二甲基喹硫氨酸二甲基氨基水解酶1调节大鼠或小鼠近端肾小管中的液体重吸收

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Nitric oxide prevents hypertension yet enhances proximal tubule Na+ reabsorption. Nitric oxide synthase is inhibited by asymmetric dimethylarginine (ADMA) that is metabolized by dimethylarginine dimethylaminohydrolase (DDAH) whose type 1 isoform is expressed abundantly in the proximal tubule (PT). We hypothesize that ADMA metabolized by DDAH-1 inhibits fluid reabsorbtion (Jv) by the proximal tubule. S2 segments of the PT were micropeifused between blocks in vivo to assess Jv in anesthetized rats. Compared with vehicle, microperfusion of ADMA or N~ω-nitro-L-arginine methyl ester (l-NAME) in the proximal tubule reduced Jv dose dependently. At 10~(-4)mol/1 both reduced Jv by ～40% (vehicle: 3.2 ± 0.7 vs. ADMA:2.1 ± 0.5, P < 0.01 vs. l-NAME: 1.9 ± 0.4 n1·min~(-1)·mm~(-1), P < 0.01; n = 10). Selective inhibition of DDAH-1 in rats with intravenous L-257 (60 mg/kg) given 2 h before and L-257 (10~(-5) mol/1) perfused in the proximal tubule for 5 min reduced Jv by 32 ± 4% (vehicle:3.2 ± 0.5 vs. L-257: 2.2 ± 0.5 nl·min~(-1)·mm~(-1); P < 0.01) and increased plasma ADMA by ≈50% (vehicle: 0.46 ± 0.03 vs. L-257: 0.67 ± 0.03 μmol/l, P < 0.0001) without changing plasma symmetric dimethylarginine. Compared with nontargeted control small-interference RNA, knock down of DDAH-1 in mice by 60% with targeted small-interference RNAs (siRNA) reduced Jv by 29 ± 5% (nontargeted siRNA: 2.8 ± 0.20 vs. DDAH-1 knockdown: 1.9 ± 0.31 nl·min~(-1)·mm~(-1), P < 0.05). In conclusion, fluid reabsorption in the proximal tubule is reduced by tubular ADMA or by blocking its metabolism by DDAH-1. L-257 is a novel regulator of proximal tubule fluid reabsorption.
机译：一氧化氮可防止高血压且增强近端小管Na + Reableplating。通过非对称二甲基碱（ADMA）抑制一氧化氮合成酶，其由二甲基甘氨酸二甲基氨基酰氯酶（DDAH）代谢，其类型1同种型在近端小管（Pt）中大量表达。我们假设DDAH-1代谢的ADMA通过近端小管抑制流体Regsorbtion（JV）。 PT的S2段在体内的嵌段之间微偏见，以评估麻醉大鼠的JV。与载体相比，在近端小管中的ADMA或N〜ω-NITRO-L-精氨酸甲酯（L-NAME）的微孔依赖性降低了JV剂量。在10〜（4）mol / 1均减少JV〜40％（车辆：3.2±0.7 Vs. ADMA：2.1±0.5，P <0.01 Vs. L-name：1.9±0.4 n1·min〜（-1 ）·mm〜（-1），p <0.01; n = 10）。在近端小管中灌注2小时的静脉内L-257（60mg / kg）的大鼠中的DDAH-1在大鼠中的选择性抑制DDAH-1（10〜（-5）摩尔/ 1）5分钟，减少了32 ±4％（车辆：3.2±0.5与L-257：2.2±0.5 nl·min〜（-1）·mm〜（-1）; p <0.01）和血浆ADMA增加≈50％（车辆：0.46 ±0.03与L-257：0.67±0.03μmol/ L，P <0.0001）而不改变等离子体对称的二甲基碱。与Nontargeted控制小干扰RNA相比，用靶向小干扰RNA（siRNA）将DDAH-1敲低DDAH-1，靶向小干扰RNA（siRNA）降低了JV（Nontargeted siRNA：2.8±0.20 Vs. DDAH-1敲低： 1.9±0.31 nl·min〜（-1）·mm〜（-1），p <0.05）。总之，近端小管中的流体重吸收通过管状氧化剂或通过DDAH-1阻断其代谢。 L-257是近端小管液重吸收的新型调节剂。

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