Bicarbonate-dependent amantadine transport by rat renal cortical proximal and distal tubules.

Transport of the achiral cationic drug amantadine by purified renal cortical rat tubules was investigated in bicarbonate [Krebs-Henseleit solution (KHS)] and nonbicarbonate buffers. Values of the apparent Km for amantadine accumulation were higher (P < .001, mean +/- S.E., n = 5) for all nonbicarbonate buffers compared with those in KHS in both proximal (76 +/- 5 in KHS, 277 +/- 65 in phosphate, 190 +/- 11 in Tris-HEPES, 268 +/- 46 in acetate and 620 +/- 81 microM in lactate) and distal tubules (68 +/- 4 in KHS, 162 +/- 27 in phosphate, 247 +/- 45 in Tris-HEPES, 281 +/- 50 in acetate buffer and 482 +/- 85 microM for lactate). There was a decrease in Vmax for amantadine transport (P < .001) in phosphate, Tris-HEPES and acetate buffers in both proximal (4.83 +/- 0.43 in KHS, 2.38 +/- 0.43 in phosphate, 1.77 +/- 0.31 in Tris-HEPES and 1.47 +/- 0.40 nmol mg protein-1 min-1 in acetate) and distal (4.58 +/- 0.13 for KHS, 1.37 +/- 0.27 for phosphate, 1.82 +/- 0.37 for Tris-HEPES and 1.76 +/- 0.20 nmol mg protein-1 min-1 for acetate) tubules. However, Vmax was not depressed (P < .09) in lactate buffer for proximal (2.87 +/- 0.24 in KHS and 3.12 +/- 0.34 nmol mg protein-1 min-1 in lactate) or distal tubules (2.42 +/- 0.26 in KHS and 3.21 +/- 0.31 nmol mg protein-1 min-1 in lactate), although a slight increase was observed in distal tubules.(ABSTRACT TRUNCATED AT 250 WORDS)