title: Characterization of Na+ transport across the cell membranes of the ascending thin limb of Henle's loop.
abstract: In the ascending thin limb of Henle's loop (ATL), intracellular Na+ is extruded by Na+/K+ ATPase in the basolateral membrane. To further characterize Na+ transport across the cell membranes of the ATL, the intracellular sodium concentration ([Na+]i) was monitored using a sodium-sensitive fluorescent probe, SBFI, in the in vitro microperfused hamster ATL. Basal [Na+]i was 19.0 +/- 1.2 mM (N = 24). Removal and replacement of luminal Na+ did not change [Na+]i in the presence of Na+ in the bathing fluid. In contrast, luminal Na+ removal reduced [Na+]i from 11.6 +/- 0.9 to 6.3 +/- 0.8 mM in the absence of peritubular Na+ (P < 0.0005, N = 21). Replacement of luminal Na+ increased [Na+]i to 12.6 +/- 0.9 mM. In the absence of Na+ in the bath, the addition of 1 microM benzamil, 0.1 mM 5-(N,N-dimethyl)-amiloride (DMA), 0.1 mM furosemide, or 0.1 mM trichlormethiazide to the lumen did not change [Na+]i or the rate of change in [Na+]i/dt) after removal and replacement of luminal Na+. Decreases in luminal pH in a Hepes-buffered solution and luminal HCO3- did not affect [Na+]i. In the absence of peritubular Na+, DMA in the bathing fluid decreased [Na+]i from 11.4 +/- 1.3 to 6.4 +/- 1.2 mM (P < 0.01, N = 5) and completely inhibited the changes in [Na+]i after removal and replacement of luminal Na+. Removal of peritubular Na+ reduced [Na+]i from 18.8 +/- 1.2 to 11.3 +/- 0.7 mM (P < 0.0001, N = 23). Addition of DMA in the bathing fluid reduced [Na+]i and inhibited the changes in [Na+]i after removal and replacement of peritubular Na+.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Clinical Biology and Hormonal Regulation, Tohoku University School of Medicine, Sendai, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Takahashi
authors.forename: Y
authors.initials: Y
authors.lastname: Kondo
authors.forename: I
authors.initials: I
authors.lastname: Fujiwara
authors.forename: O
authors.initials: O
authors.lastname: Ito
authors.forename: Y
authors.initials: Y
authors.lastname: Igarashi
authors.forename: K
authors.initials: K
authors.lastname: Abe
mesh_terms: D000584:Amiloride / Q000031:analogs & derivatives / Q000494:pharmacology; D000818:Animals; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism; D002463:Cell Membrane Permeability; D006224:Cricetinae; D005665:Furosemide / Q000494:pharmacology; D006863:Hydrogen-Ion Concentration; D066298:In Vitro Techniques; D007424:Intracellular Fluid / Q000187:drug effects / Q000378:metabolism; D008138:Loop of Henle / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D008647:Mesocricetus; D012964:Sodium / Q000378:metabolism*; D017923:Sodium-Hydrogen Exchangers / Q000187:drug effects / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000187:drug effects / Q000378:metabolism; D014237:Trichlormethiazide / Q000494:pharmacology
chemical_list: D017923:Sodium-Hydrogen Exchangers; C013407:benzamil; C039465:5-dimethylamiloride; D000584:Amiloride; D005665:Furosemide; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D014237:Trichlormethiazide