The distal tubule isn't nearly as exciting or as clearly well defined as the proximal tubule. As you go from the end of the loop of Henle (the thick ascending limb) towards the collecting duct, the distal tubule cells gradually change from being practically indistinguishable from those of the loop of Henle to being practically indistinguishable from those of the cortical collecting duct. The latter part of the distal tubule and the beginning of the collecting duct are the main site of action of aldosterone (remember the renin-angiotensin-aldosterone system) which acts to increase sodium reabsorption. The main cell type in this part of the nephron are called principle cells, these cells are crammed full of mitochondria and have a huge sodium pump activity. Aldosterone is a steroid hormone and, like other steroid hormones, it can penetrate the cell membrane and so have a direct effect on cellular mechanisms. Aldosterone increases sodium pump synthesis. This is obviously a good way of increasing sodium reabsorption, furthermore, protein synthesis takes time, such a mechanism would explain why there is a delay (at least 30 minutes) before aldosterone has any detectable effect on renal function. There is another cell type in the distal tubule, the intercalated cells. These have little sodium pump activity, but lots of carbonic anhydrase activity. These cells represent the last stop for bicarbonate reabsorption. They reabsorb bicarbonate in almost the same was as the proximal tubule cells except that they use a proton pump rather than sodium/proton exchange to export protons. This allows them to operate against high pH gradients (The urine can be highly acidic by this point, pH = 4.5 or a proton concentration about 1000 times that of plasma).