Ullrich K J, Fasold H, Rumrich G, Klöss S
Pflugers Arch. 1984 Mar;400(3):241-9. doi: 10.1007/BF00581554.
The transport of dicarboxylic acids in the proximal convolution was investigated by measuring: a) the zero net flux transtubular concentration difference of DL-methyl-succinate, b) its 2-s influx from the interstitium into tubular cells, and c) its 3.5-s efflux from the tubular lumen. With the first method a luminal concentration exceeding the peritubular concentration was observed, thus indicating a net active transtubular secretion of this slowly metabolized substance. All transport steps, luminal and contraluminal , as well as the overall transport, were Na+-dependent and inhibited by lithium (apparent Ki approximately equal to 1.8 mmol/l). The overall transport of methylsuccinate , as well as the contraluminal influx into proximal tubular cells, could be inhibited by paraaminohippurate and H2-DIDS with an apparent Ki of approximately equal to 1.8 mmol/l, by taurocholate with an apparent Ki approximately equal to 3.1 mmol/l and by pyruvate with an apparent Ki approximately equal to 5 mmol/l, but not by sulfate, thiosulfate, L-lactate, oxalate and urate. As judged from the inhibition of contraluminal methylsuccinate influx by 48 dicarboxylic acids (aliphatic and aromatic), a specificity pattern was observed similar to that of inhibition of luminal efflux of 2-oxoglutarate [22]: a preference of dicarboxylates in the transconfiguration with a chain length of 4-5 carbons; little change in the inhibitory potency with CH3-, OH-, SH- and O=, but strong reduction with a NH3+ in the 2 position; only a small reduction of inhibitory potency with 2,3 disubstituted SH and OH analogs; preference of the dicarboxylic benzene in the 1,4 position and of the diacetyl benzene in the 1,2 position. The data indicate a Na+-dependent dicarboxylic transport system at the contraluminal cell side of the proximal tubule which is very similar to the luminal transport system for dicarboxylic acids.
通过测量以下各项,研究了近端曲管中二羧酸的转运:a)DL-甲基琥珀酸的零净通量跨管浓度差,b)其从间质到肾小管细胞的2秒内流,以及c)其从肾小管腔的3.5秒外流。使用第一种方法观察到管腔浓度超过管周浓度,因此表明这种代谢缓慢的物质存在净主动跨管分泌。所有转运步骤,管腔和管腔对侧的,以及整体转运,均依赖于Na+并受锂抑制(表观Ki约等于1.8 mmol/L)。甲基琥珀酸的整体转运以及向近端肾小管细胞的管腔对侧内流,可被对氨基马尿酸和H2-DIDS抑制,表观Ki约等于1.8 mmol/L,被牛磺胆酸盐抑制,表观Ki约等于3.1 mmol/L,被丙酮酸抑制,表观Ki约等于5 mmol/L,但不受硫酸盐、硫代硫酸盐、L-乳酸、草酸盐和尿酸盐抑制。根据48种二羧酸(脂肪族和芳香族)对管腔对侧甲基琥珀酸内流的抑制作用判断,观察到的特异性模式与2-氧代戊二酸管腔外流的抑制模式相似[22]:反式构型中链长为4-5个碳的二羧酸盐具有偏好性;CH3-、OH-、SH-和O=取代时抑制效力变化不大,但2位有NH3+时抑制效力大幅降低;2,3-二取代的SH和OH类似物的抑制效力仅略有降低;1,4位的二羧酸苯和1,2位的二乙酰苯具有偏好性。数据表明近端小管管腔对侧细胞侧存在依赖于Na+的二羧酸转运系统,该系统与二羧酸的管腔转运系统非常相似。