Contribution of Na+-H+ exchange to sodium reabsorption in the loop of Henle: a microperfusion study in rats

1. The contribution of apical Na+-H+ exchange to sodium reabsorption in the thick ascending limb of the loop of Henle (TALH) in vivo was examined in a naesthetized rats by perfusing loops of Henle of superficial nephrons with solutions containing the Na+-H+ exchange inhibitor, ethyl isopropyl amilori de (EIPA). 2. Using a standard perfusate, no statistically significant effect of EIPA on net sodium reabsorption (J(Na)) was detected. However, when sodium reabs orption in the pars recta of the proximal tubule was minimized by using a l ow-sodium perfusate, EIPA reduced J(Na) from 828 +/- 41 to 726 +/- 37 pmol min(-1) (P < 0.05), indicating that apical Na+-H+ exchange can make a small contribution to net sodium reabsorption in the TALH in vivo. This contribu tion appears to be dependent on the bicarbonate load, since an increase in the latter led to an enhancement of EIPA-sensitive sodium transport. 3. Addition of the Na+-K+-2Cl(-) cotransport inhibitor, bumetanide, to the low-sodium perfusate reduced baseline J(Na) to 86 +/- 27 pmol min(-1). In t his setting, EIPA reduced J(Na) further, to -24 +/- 18 pmol min(-1) (P < 0. 05), an effect similar to that seen in the absence of bumetanide. This find ing argues against previous suggestions (based on in vitro evidence) that i nhibition of the Na+-K+-2Cl(-) cotransporter leads to an increase in apical Na+-H+ exchange in the TALH.