TY - JOUR
T1 - Tetraethylammonium transport by isolated perfused snake renal tubules
AU - Hawk, C. T.
AU - Dantzler, W. H.
PY - 1984
Y1 - 1984
N2 - Tetraethylammonium (TEA) transport was studied in isolated perfused snake (Thamnophis spp.) proximal renal tubules. Unidirectional lumen-to-bath (J (TEA)(1→b)) and bath-to-lumen (J (TEA)(1→b)) fluxes exhibited saturation kinetics, but J(TEA)(b→ 1) also exhibited an apparent diffusive component and J(TEA)(1 → b) did not. J(TEA)(b→ 1) exceeded J(TEA)(1→b) at all concentrations studied, resulting in net TEA secretion. Transport into cells across both luminal and peritubular membranes was apparently against an electrochemical gradient and was inhibited by cyanide. K(m) for J(TEA)(1→b) (5.9 μM) was about one-third K(m) for J(TEA)(b→ 1)) (19.9 μM), indicating greater affinity of the luminal transporter for TEA; but V(max) for J(TEA)(b→ 1) (153 fmol·min-1·mm-1) was about six times V(max) for J(TEA)(1→b)) (27 fmol·min-1), indicating a greater capacity of the peritubular transporter for TEA, which could account for net TEA secretion. J(TEA)(b→ 1) was inhibited by N-methylnicotinamide (NMN) in the bath, but J(TEA)(1→b) was inhibited initially and then apparently transstimulated by NMN in the lumen, indicating possible countertransport. J(TEA)(1→b), but not J(TEA)(b→ 1), was significantly reduced by replacement of sodium with sucrose, indicating possible sodium dependency of the luminal transporter. All data indicate active (either primary or secondary) TEA transport at both luminal and peritubular membranes but net transepithelial transport in the bath-to-lumen direction.
AB - Tetraethylammonium (TEA) transport was studied in isolated perfused snake (Thamnophis spp.) proximal renal tubules. Unidirectional lumen-to-bath (J (TEA)(1→b)) and bath-to-lumen (J (TEA)(1→b)) fluxes exhibited saturation kinetics, but J(TEA)(b→ 1) also exhibited an apparent diffusive component and J(TEA)(1 → b) did not. J(TEA)(b→ 1) exceeded J(TEA)(1→b) at all concentrations studied, resulting in net TEA secretion. Transport into cells across both luminal and peritubular membranes was apparently against an electrochemical gradient and was inhibited by cyanide. K(m) for J(TEA)(1→b) (5.9 μM) was about one-third K(m) for J(TEA)(b→ 1)) (19.9 μM), indicating greater affinity of the luminal transporter for TEA; but V(max) for J(TEA)(b→ 1) (153 fmol·min-1·mm-1) was about six times V(max) for J(TEA)(1→b)) (27 fmol·min-1), indicating a greater capacity of the peritubular transporter for TEA, which could account for net TEA secretion. J(TEA)(b→ 1) was inhibited by N-methylnicotinamide (NMN) in the bath, but J(TEA)(1→b) was inhibited initially and then apparently transstimulated by NMN in the lumen, indicating possible countertransport. J(TEA)(1→b), but not J(TEA)(b→ 1), was significantly reduced by replacement of sodium with sucrose, indicating possible sodium dependency of the luminal transporter. All data indicate active (either primary or secondary) TEA transport at both luminal and peritubular membranes but net transepithelial transport in the bath-to-lumen direction.
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U2 - 10.1152/ajprenal.1984.246.4.f476
DO - 10.1152/ajprenal.1984.246.4.f476
M3 - Article
C2 - 6232857
AN - SCOPUS:18244428822
SN - 0363-6143
VL - 15
SP - F476-F487
JO - American Journal of Physiology - Renal Fluid and Electrolyte Physiology
JF - American Journal of Physiology - Renal Fluid and Electrolyte Physiology
IS - 4
ER -