Ullrich K J, Papavassiliou F
Pflugers Arch. 1981 Mar;389(3):271-5. doi: 10.1007/BF00584789.
Using the technique of capillary perfusion and simultaneous luminal stop flow microperfusion the reabsorption of bicarbonate and glycodiazine from the papillary collecting duct was evaluated. Starting with equal H14CO3- and 3H-glycodiazine concentrations in the luminal and peritubular perfusates, the decrease in the luminal concentration at 10 and 45 s contact time was measured. In control rats with 25 mmol/l HCO3- in the perfusates the rate of HCO3- reabsorption calculated from the 10 s values was 0.34 nmol cm-2 s-1. In acute metabolic acidosis, the rate of bicarbonate reabsorption was 2,3 times higher. In metabolic alkalosis, the rate of bicarbonate absorption dropped to 13% of the control values. Also the 45 s values of acidotic and alkalotic animals differed significantly from each other. With 25 mmol/l glycodiazine in both perfusates the rate of buffer reabsorption as calculated from the 10 s values was 0.76 nmol cm-2 s-1 in control rats and did not deviate significantly from this value in acidotic and alkalotic animals. In control rats the bicarbonate reabsorption in % was the same, no matter whether both luminal and capillary perfusate contained 25 mmol/l bicarbonate or 10 mmol/l. In acidotic rats the rate of HCO3- reabsorption did not change significantly if all Na+ in the perfusates was replaced by choline (0.88 versus 0.79 nmol cm-2 s-1 at 25 mmol/l HCO3-). When in acidotic rats. 0.1 mmol/l acetazolamide or 1 mmol/l SITS (4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic acid) was added to both perfusates the rate of HCO3- reabsorption dropped by 75 and 58%, respectively. A potassium deficient diet for one week and DOCa administration had no influence on the bicarbonate reabsorption of rats which were on standard diet. The data indicate that (1) the buffer reabsorption from the papillary collecting duct is rather due to H+ ion secretion than to buffer anion reabsorption. (2) The adaptation to metabolic acidosis and alkalosis is specific for bicarbonate and not seen with glycodiazine. (3) Within the concentration range tested the HCO3- reabsorption rises linearly with the HCO3- concentration. (4) The HCO3- reabsorption in the papillary collecting duct is Na+-independent, it can be inhibited by acetazolamide and SITS, but is not influenced by K+-deficient diet plus DOCA.
采用毛细血管灌注技术和同时进行的管腔停流微灌注技术，评估了乳头集合管中碳酸氢盐和甘氨二嗪的重吸收情况。起始时管腔和肾小管周围灌注液中H14CO3-和3H-甘氨二嗪浓度相等，测量了接触时间为10秒和45秒时管腔浓度的降低情况。在灌注液中含有25 mmol/l HCO3-的对照大鼠中，根据10秒时的值计算出的HCO3-重吸收率为0.34 nmol cm-2 s-1。在急性代谢性酸中毒时，碳酸氢盐重吸收率高出2.3倍。在代谢性碱中毒时，碳酸氢盐吸收率降至对照值的13%。酸中毒和碱中毒动物的45秒时的值也有显著差异。当两种灌注液中均含有25 mmol/l甘氨二嗪时，根据10秒时的值计算出的对照大鼠中缓冲剂重吸收率为0.76 nmol cm-2 s-1，酸中毒和碱中毒动物的该值与对照值无显著偏差。在对照大鼠中，无论管腔和毛细血管灌注液中含有25 mmol/l碳酸氢盐还是10 mmol/l，碳酸氢盐重吸收的百分比都是相同的。在酸中毒大鼠中，如果灌注液中的所有Na+被胆碱替代，HCO3-重吸收率无显著变化（25 mmol/l HCO3-时分别为0.88和0.79 nmol cm-2 s-1）。当在酸中毒大鼠的两种灌注液中添加0.1 mmol/l乙酰唑胺或1 mmol/l SITS（4-乙酰氨基-4'-异硫氰酸基芪-2,2'-二磺酸）时，HCO3-重吸收率分别下降75%和58%。一周的低钾饮食和给予地塞米松对标准饮食大鼠的碳酸氢盐重吸收无影响。这些数据表明：（1）乳头集合管中的缓冲剂重吸收更多是由于H+离子分泌而非缓冲阴离子重吸收。（2）对代谢性酸中毒和碱中毒的适应是碳酸氢盐特有的，甘氨二嗪未见此现象。（3）在所测试的浓度范围内，HCO3-重吸收随HCO3-浓度呈线性增加。（4）乳头集合管中的HCO3-重吸收不依赖于Na+，可被乙酰唑胺和SITS抑制，但不受低钾饮食加地塞米松的影响。
