Brezis M, Spokes K, Silva P, Epstein F H
Am J Physiol. 1986 Nov;251(5 Pt 2):F873-8. doi: 10.1152/ajprenal.1986.251.5.F873.
The effect of exogenous metabolic substrates on K+ secretion was evaluated in the isolated perfused rat kidney in the presence of 2-deoxyglucose and 2-tetradecylglycidic acid to inhibit utilization of glucose and fatty acids from endogenous sources. L-Lactate (15 mM) added to the perfusion medium enhanced renal oxygen consumption (4.0 +/- 1.1 mumol X min-1 X g-1 vs. 2.0 +/- 1.0 without lactate) while decreasing fractional excretion of sodium (19.3 +/- 2.4% vs. 47.3 +/- 1.8). L-Lactate markedly increased the fractional excretion of K+ to 181 +/- 29% compared with 68 +/- 12% without lactate (P less than 0.001). The poorly metabolized isomer D-lactate did not alter these parameters. The addition of alpha-ketoglutarate only slightly increased K+ excretion. In the absence of metabolic inhibitors and in the presence of glucose (5 mM), L-lactate also increased K+ excretion significantly more than did D-lactate (108 +/- 19% vs. 69 +/- 11, P less than 0.02). At the end of 90 min of perfusion with L-lactate medium, K+ concentration in the perfusate dropped from 4.7 +/- 0.05 to 3.2 +/- 0.2 meq/liter (vs. 3.8 +/- 0.1 meq/liter with D-lactate, P less than 0.005) without differences in glomerular filtration rate or sodium excretion. L-Lactate appears to increase K+ secretion by preferential metabolic stimulation of the distal tubule, a process that may help in vivo to prevent hyperkalemia in lactic acidosis.
在存在2-脱氧葡萄糖和2-十四烷基甘油酸以抑制内源性葡萄糖和脂肪酸利用的情况下，在离体灌注大鼠肾脏中评估外源性代谢底物对钾分泌的影响。添加到灌注培养基中的L-乳酸（15 mM）可增强肾脏耗氧量（4.0±1.1 μmol·min⁻¹·g⁻¹，而无乳酸时为2.0±1.0），同时降低钠的分数排泄率（19.3±2.4%，而无乳酸时为47.3±1.8%）。与无乳酸时的68±12%相比，L-乳酸显著增加钾的分数排泄率至181±29%（P<0.001）。代谢较差的异构体D-乳酸不会改变这些参数。添加α-酮戊二酸仅略微增加钾排泄。在不存在代谢抑制剂且存在葡萄糖（5 mM）的情况下，L-乳酸也比D-乳酸显著更多地增加钾排泄（108±19%对69±11，P<0.02）。在用L-乳酸培养基灌注90分钟结束时，灌注液中的钾浓度从4.7±0.05降至3.2±0.2 meq/升（而用D-乳酸时为3.8±0.1 meq/升，P<0.005），肾小球滤过率或钠排泄无差异。L-乳酸似乎通过对远端小管的优先代谢刺激来增加钾分泌，这一过程可能在体内有助于预防乳酸酸中毒时的高钾血症。
