Harris D C, Tay C
Department of Renal Medicine, Westmead Hospital, N.S.W., Australia.
Nephron. 1993;64(3):417-23. doi: 10.1159/000187364.
To understand further the contribution of heightened net sodium reabsorption (TNa+) and other nontransport processes to increased and altered metabolic activity of the rat remnant kidney (RK), isolated RK and normal kidneys (NK) were perfused with and without metabolic inhibitors and following 4 weeks of low (12%)- or high (40%)-protein diet. 3-Mercaptopicolinate (200 microM) and 2-deoxyglucose (200 microM) reduced glucose production and consumption, respectively, without altering oxygen consumption (QO2). Ouabain reduced TNa+ and QO2 in NK but not RK, and increased glucose consumption in RK (by 67%, p < 0.02, n = 12) and NK (by 54%, p < 0.05, n = 12). Raising perfusate pH by 0.3 U to 7.65 increased glucose production in RK but not NK and reduced TNa+ in NK but not RK. Dietary protein restriction reduced QO2 (2.18 +/- 0.29 vs. 4.13 +/- 0.20 mumol-1 x min-1 x g-1, p < 0.001), TNa+ (8.74 +/- 4.39 vs. 38.83 +/- 8.32, p < 0.01) and ammoniagenesis (0-30 min, 0.16 +/- 0.05 vs. 0.32 +/- 0.10, p < 0.05) in RK, but not NK. In summary: (1) responses to ouabain and alkalosis, but not other metabolic inhibitors, were quite distinct in remnant versus normal kidneys, and (2) protein restriction limited sodium-transport-dependent and -independent hypermetabolism in RK.
为了进一步了解净钠重吸收增加（TNa +）和其他非转运过程对大鼠残余肾（RK）代谢活性增加和改变的作用，分别用代谢抑制剂和不用代谢抑制剂灌注分离的RK和正常肾（NK），并给予低蛋白（12%）或高蛋白（40%）饮食4周。3 - 巯基吡啶甲酸盐（200 microM）和2 - 脱氧葡萄糖（200 microM）分别降低了葡萄糖生成和消耗，而不改变氧消耗（QO2）。哇巴因降低了NK中的TNa +和QO2，但对RK无此作用，且增加了RK中的葡萄糖消耗（增加67%，p < 0.02，n = 12）和NK中的葡萄糖消耗（增加54%，p < 0.05，n = 12）。将灌注液pH提高0.3单位至7.65增加了RK中的葡萄糖生成，但对NK无此作用，降低了NK中的TNa +，但对RK无此作用。饮食蛋白限制降低了RK中的QO2（2.18±0.29对4.13±0.20微摩尔-1×分钟-1×克-1，p < 0.001）、TNa +（8.74±4.39对38.83±8.32，p < 0.01）和氨生成（0 - 30分钟，0.16±0.05对0.32±0.10，p < 0.05），但对NK无此作用。总之：（1）残余肾与正常肾对哇巴因和碱中毒的反应（但不是对其他代谢抑制剂的反应）有很大差异，（2）蛋白限制限制了RK中钠转运依赖性和非依赖性的高代谢。
