Electrical properties of sodium bicarbonate symport in kidney epithelial cells (BSC-1)

Abstract

Intracellular potentials of BSC-1 kidney epithelial cells known to express a Na+-HCO3- symport ranged between -40 and -70 mV, mean value Vm = -55.1 +/- 10.1 mV. Lowering HCO3- at constant partial pressure of CO2 (PCO2) or complete removal of HCO3-/CO2, rapidly depolarized, whereas readding HCO3- hyperpolarized Vm (40 +/- 8 mV/decade HCO3- at constant PCO2). This response was largely reduced by 1 mM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) (which depolarized Vm to about -20 mV) and in Na+-free medium, but Ba2+ had no effect. In HCO3(-)-Ringer, Na+ removal rapidly depolarized Vm (by 32 +/- 7 mV), and readdition hyperpolarized Vm. This was reduced in HCO3(-)-free medium or by 1 mM DIDS, but not by amiloride (10(-5) and 10(-3) M) or ouabain (10(-4) M). In the absence of HCO3- and/or Na+, steady-state Vm was reduced to -12 +/- 5 mV. Cl- removal had no effect on the responses to Na+ and/or HCO3- and led to a slow steady-state depolarization. Both in the presence and absence of HCO3-, raising pHi (changed by NH4Cl or butyrate) depolarized, whereas lowering pHi hyperpolarized Vm. Lowering pHo in HCO3(-)-free Ringer depolarized Vm (23 +/- 4 mV/decade H+). The slope conductance for K+ is only 6 +/- 2 mV/decade. Thus BSC-1 cells display typical electrical characteristics of Na+-HCO3- symport. In contrast to other systems, the data are compatible with a net electrogenic inward transport of Na+ and HCO3-. There might be an additional H+-(OH-) conductance operating also under nominally bicarbonate-free conditions.

Parallel adaptation of the rabbit renal cortical sodium/proton antiporter and sodium/bicarbonate cotransporter in metabolic acidosis and alkalosis.

“…Bicarbonate absorption by proximal renal tubules is considered to be mediated by Na+/H' exchange and perhaps H+-dependent ATPase in the apical membranes (20,36), and Na+/ HCO3 cotransport (9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19) and 14CO3/Cl-exchange (35,42) in the basolateral membrane. Of these transporters, the Na+/H' antiporter in the brush border membrane and Nae/HCO3 cotransporter in the basolateral membrane are considered to play major roles in regulating the intracellular pH ofproximal tubular cells (17).…”

“…Recently a sodium/bicarbonate cotransporter has been described in basolateral membrane vesicles prepared from rabbit renal cortex (9,10). This transporter plays a significant role in bicarbonate reabsorption and regulation of intracellular pH in the proximal tubular cell (11)(12)(13)(14)(15)(16)(17)(18)(19). The factors that regulate the activity of this transporter have not yet been identified.…”

Kinetic properties and Na+ dependence of rheogenic Na(+)‐HCO3‐ co‐transport in frog retinal pigment epithelium.

“…In the cultured BSC-1 cells (Jentsch, Matthes, Keller & Wiederholt, 1986b) and in frog retinal pigment epithelial cells (Hughes et al 1989) a stoichiometry of Na+-HCO3-co-transport of 1:2 has been reported. In BSC-1 cells a kinetic analysis of the sodium dependence of Na+-HCO3-co-transport at constant extracellular pH, but different HCO3-concentrations showed that the affinity constant (Km) for sodium increased with decreasing extracellular HCO3-concentrations (Jentsch, Schwartz, Schill, Langer, Lepple, Keller & Wiederholt, 1986a).…”

Stoichiometry of Na+-HCO-3 cotransport in basolateral membrane vesicles isolated from rabbit renal cortex.

“…Boron and Boulpaep described a process of Na+-HCO3 cotransport across the basolateral membrane of the amphibian proximal tubule (2). Recent studies suggest that this transport process is also the major mechanism for exit of HCO3 across the basolateral membrane of the mammalian proximal tubule cell (3)(4)(5)(6)(7)(8)(9)(10). In addition, Na'-HCO-cotransport has been observed in corneal endothelial cells (1 1, 12), suggesting that this pathway is involved in mediating HCO-transport in epithelial tissues other than the kidney.…”