PTH-sensitive K(+)- and voltage-dependent Pi transport by chick renal brush-border membranes.

Brush-border membrane vesicles (BBMV) from chick (Gallus gallus) kidneys were used to examine possible pathways of Pi transport associated with Pi secretion. Preloading with 6 mM Pi trans-stimulated 32Pi uptake in the absence of Na+, indicating facilitation. Inside-positive voltage (100 mM K+, out > in, +valinomycin) increased Pi uptake from 161 +/- 4.4 to 241 +/- 16.1 pmol.mg protein-1.5s-1 at pH 7.5 (in = out). Gradients characterized by extravesicular pH (pHo) of 5.5 vs. intravesicular pH (pHi) of 7.5, 100 mM K+ (out > in), without and with valinomycin, further increased uptake to 664 +/- 148.5 and 946 +/- 90.8 pmol.mg protein-1.5s-1, respectively. Carbonyl cyanide m-chlorophenylhydrazone (CCCP) had no effect on the latter response, but with 100 mM K+ (in = out), valinomycin decreased the response more than one-half, implicating a H+ diffusion potential. Generation of this potential with pHo 5.5 vs. pHi 7.5 and CCCP did not drive concentrative Pi uptake in absence of K+. Parathyroid hormone (PTH) treatment significantly increased this BBMV K(+)- and voltage-dependent Pi up-take compared with the parathyroidectomized (PTX) condition. The values of maximal uptake rate (Vmax) in PTH vs. PTX BBMV were 5,330 and 1,976 pmol.mg protein-1.5s-1, respectively. K(+)-dependent transport was inhibited by arsenate, phosphonoacetic acid, and vanadate. Together, the data indicate that this PTH-sensitive, voltage- and K(+)-dependent monovalent Pi transporter could be the mechanism by which Pi exits, cell-to-lumen, during renal tubular Pi secretion.