Renal bicarbonate reabsorption in the rat. IV. Bicarbonate transport mechanisms in the early and late distal tubule.

Abstract

Bicarbonate transport was studied in vivo by separate microperfusion experiments of early and late distal tubules. Total CO2 was measured by microcalorimetry and fluid absorption by 3H-inulin. Significant bicarbonate absorption was observed in all experimental conditions. Bicarbonate transport was loaddependent upon increasing the luminal bicarbonate concentration from 15 to 50 mM in both early and late distal tubule segments and remained constant at higher concentrations at a maximum rate of 100-110 pmol/min per mm. At low lumen bicarbonate concentrations (15 mM), higher rates of bicarbonate absorption were observed in early (32.9±4.57 pmol/min per mm) as compared to late distal tubules (10.7±3.1 pmol/ min per mm). Amiloride and ethyl-isopropylamiloride both inhibited early but not late distal tubule bicarbonate absorption whereas acetazolamide blocked bicarbonate transport in both tubule segments. Fluid absorption was significantly reduced in both tubule segments by amiloride but only in early distal tubules by ethyl-isopropylamiloride. Substitution of lumen chloride by gluconate increased bicarbonate absorption in late but not in early distal tubules. Bafilomycin Al, an inhibitor of HATPase, inhibited late and also early distal tubule bicarbonate absorption, the latter at higher concentration. After 8 d on a low K diet, bicarbonate absorption increased significantly in both early and late distal tubules. Schering compound 28080, a potent H-K ATPase inhibitor, completely blocked this increment of bicarbonate absorption in late but not in early distal tubule. The data suggest bicarbonate absorption via Na+-H+ exchange and H-ATPase in early, but only by amiloride-insensitive H' secretion (H-ATPase) in late distal tubules. The study also provides evidence for activation of K+-H+ exchange in late distal tubules of K depleted rats. Indirect evidence implies a component of chloride-dependent bicarbonate secretion in late distal tubules and suggests that net bicarbonate transport at this site results from bidirectional bicarbonate movement. (J. Clin.

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“…ANP does not affect bicarbonate reabsorption in either segment and, as opposed to what was seen in the proximal tubule, does not impair the stimulation caused by ANG II. This result is in accordance with data indicating that in ED segments bicarbonate reabsorption is mediated predominantly by Na + /H + exchange and in LD segments by vacuolar H + -ATPase (17,18) and with studies that indicate the absence of ANP receptors in distal segments (19). The present study, however, does not allow us to ascribe the results with ANG II to any specific cell type that might contribute to acidification in cortical distal tubules.…”

Endogenous endothelins mediate increased distal tubule acidification induced by dietary acid in rats.

“…ET-1 also stimulates the Na ϩ /H ϩ exchanger in renal cortical membrane vesicles (37) and the NHE-3 isoform in renal epithelial cells (8), supporting a possible endothelin role in modulating renal acidification in vivo. The NHE performs much of the H ϩ secretion in the rat distal tubule accessible to micropuncture (38). ET-1 also inhibits agonist-stimulated increases in cellular cyclic AMP levels in renal epithelium (36), a cellular second messenger whose increase is associated with augmented HCO 3 secretion in cortical collecting tubules (39) and with inhibited NHE activity in renal brush border membranes (40).…”

Integrated Control of Na Transport along the Nephron

“…In the early DCT, Na reabsorption is largely sensitive to thiazide diuretics, implicating the NaCl-cotransporter NCC. In addition, this segment can reabsorb HCO 3 2 through an Na-H exchange process mediated by NHE2 (20), although this accounts for only about 10% of Na reabsorption in the DCT (21,22). In the late DCT, Na reabsorption is sensitive to amiloride (16), indicating transport through the epithelial Na channel (ENaC).…”