Yohkazu Matsushima

Stimulatory Effect of Calcium Ions on p-Aminohippurate Accumulation by Rat Kidney Cortical Slices

The effect of external Ca2+ on p-aminohippurate (PAH) transport was examined using rat kidney cortical slices. External Ca2+ increased the initial rate of PAH uptake, markedly enhanced its maximal accumulation at steady-state conditions and depressed the efflux. Kinetic studies revealed that increasing external Ca2+ from 0 to 2.5 mM resulted in an increase in the Vmax of transport, while the apparent Km values remained constant. When the intracellular Na+ levels of the slices were equal, PAH accumulation was increased in the presence of Ca2+. A divalent cation such as Ba2+, Mn2+ or Sr2+ enhanced PAH accumulation to at least the same degree as Ca2+. While Mg2+ had no effect, La3+ exhibited a little stimulatory effect on the PAH accumulation. We suggest that the stimulatory action of Ca2+ on PAH accumulation is in part dissociated from that of Na+ gradient and that Ca2+ can be substituted by Ba2+, Mn2+ and Sr2+ with regard to the stimulation of PAH accumulation.

Dissipation by tetraethylammonium of verapamil-stimulated p-aminohippurate accumulation in rat kidney cortical slices

The stimulatory effect of verapamil on p-aminohippurate (PAH) accumulation was studied in rat kidney cortical slices. PAH accumulation was stimulated by the presence of 0.3 mM verapamil in the incubation medium, but this stimulatory action of verapamil was dissipated by adding tetraethylammonium (TEA) to the medium. TEA accumulation by the kidney cortical slices was inhibited by verapamil in a concentration-dependent fashion. In addition, kinetic studies revealed that verapamil resulted in an increase in the Michaelis constant (Km) of TEA transport, with the Vmax remaining constant, suggesting that verapamil competitively inhibited TEA transport. These results suggest that the transport system for verapamil is the same as that for TEA and that verapamil taken up within the cells may stimulate PAH transport.