Nagami G T
Nephrology Section, Veterans Administration Medical Center West Los Angeles, California 90073.
J Clin Invest. 1988 Jan;81(1):159-64. doi: 10.1172/JCI113287.
A major portion of the total ammonia (tNH3 = NH3 + NH+4) produced by the isolated perfused mouse proximal tubule is secreted into the luminal fluid. To assess the role of Na+-H+ exchange in net tNH3 secretion, rates of net tNH3 secretion and tNH3 production were measured in proximal tubule segments perfused with control pH 7.4 Krebs-Ringer bicarbonate (KRB) buffer or with modified KRB buffers containing 10 mM sodium and 0.1 mM amiloride. Net tNH3 secretion was inhibited by 90% in proximal tubule segments perfused with the pH 7.4 modified KRB buffer while tNH3 production remained unaffected. The inhibition of net tNH3 secretion by perfusion with the modified KRB buffer was only partially reversed by acidifying the modified KRB luminal perfusate from 7.4 to as low as 6.2. These data indicate that the Na+-H+ exchanger facilitates a major portion of net tNH3 secretion by the proximal tubule and that luminal acidification may play only a partial role in the mechanism by which the Na+-H+ exchanger mediates net tNH3 secretion.
分离灌注的小鼠近端小管产生的总氨（tNH3 = NH3 + NH+4）的大部分分泌到管腔液中。为了评估Na+-H+交换在tNH3净分泌中的作用，在灌注对照pH 7.4的 Krebs-Ringer碳酸氢盐（KRB）缓冲液或含有10 mM钠和0.1 mM氨氯吡咪的改良KRB缓冲液的近端小管节段中测量tNH3净分泌率和tNH3产生率。在用pH 7.4改良KRB缓冲液灌注的近端小管节段中，tNH3净分泌受到90%的抑制，而tNH3产生不受影响。用改良KRB缓冲液灌注对tNH3净分泌的抑制作用仅通过将改良KRB管腔灌注液的pH从7.4酸化至低至6.2而部分逆转。这些数据表明，Na+-H+交换体促进了近端小管tNH3净分泌的大部分，并且管腔酸化在Na+-H+交换体介导tNH3净分泌的机制中可能仅起部分作用。
