We microperfused the loop of Henle (LOH) to assess its contribution to urine acidification in vivo. Under control conditions (Na HCO3- = 13 mM, perfusion rate ∼ 17 nl/min-1) net bicarbonate transport (JHCO3-) was unsaturated, flow- and concentration-dependent, and increased linearly until a bicarbonate load of 1,400 pmol·min-1 was reached. Methazolamide (2 · 10-4 M) reduced JHCO3 by 70%; the amiloride analogue ethylisopropylamiloride (EIPA) (2 · 10-4 M) reduced JHCO3 by 40%; neither methazolamide nor EIPA affected net water flux (Jv). The H+-ATPase inhibitor bafilomycin A1 (10-5 M) reduced JHCO3 by 20%; the Cl- channel inhibitor 5-nitro-2′-(3-phenylpropylamino)-benzoate (2 · 10-4 M) and the Cl--base exchange inhibitor diisothiocyanato-2,2′-stilbenedisulfonate (5 · 10-5 M), had no effect on fractional bicarbonate reabsorption. Bumetanide (10-6 M) stimulated bicarbonate transport (net and fractional JHCO3) by 20%, whereas furoscmide (10-4 M) had no effect on bicarbonate reabsorption; both diuretics reduced Jv. In summary: (a) the LOH contributes significantly to urine acidification. It normally reabsorbs an amount equivalent to 15% of filtered bicarbonate; (b) bicarbonate reabsorption is not saturated; (c) Na+-H+ exchange and an ATP-dependent proton pump are largely responsible for the bulk of LOH bicarbonate transport.
CITATION STYLE
Capasso, G., Unwin, R., Agulian, S., & Giebisch, G. (1991). Bicarbonate transport along the loop of Henle I. Microperfusion studies of load and inhibitor sensitivity. Journal of Clinical Investigation, 88(2), 430–437. https://doi.org/10.1172/JCI115322
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