pH gradient-dependent increased Na+-H+ antiport capacity of the rabbit remnant kidney.

The adaptative response of the renal proximal tubule to a reduction of renal mass was studied in brush border membrane vesicles prepared from the solitary remnant kidney (RK) of subtotally nephrectomized rabbits. The in vivo acid-base status of RK and sham-operated controls (SK) was similar. In the absence of organic solutes, Na+ flux across the membrane demonstrated features of Na+-H+ antiport, i.e., stimulation by a transmembrane pH gradient and inhibition by amiloride. Kinetic parameters for Na+-H+ antiport were derived with different experimental protocols. In the presence of an opposing H+ gradient and over a limited range of Na+ concentration, JNamax was enhanced 65% in RK vesicles compared with SK vesicles and KtNa was unchanged. The enhanced JNamax was not apparent under H+ equilibrium conditions, Comparable values for JNamax and KtNa were obtained by studying RK vesicles at external Na+ concentrations of 0-200 mM and resolving uptake into a substrate component, representing Na+-H+ antiport, and a nonsaturable diffusive component. The apparent Na+ permeability (P'Na) of RK vesicles was identical to the P'Na of normal kidney vesicles, under both H+ gradient and H+ equilibrium conditions. H+ permeability, measured with acridine orange, was also the same in RK and SK vesicles. These studies demonstrate that in the remnant kidney model of chronic renal insufficiency there is an increase in the JNamax of the Na+-H+ antiporter in the luminal membrane of the proximal tubule that is revealed only under transmembrane H+ gradient conditions.(ABSTRACT TRUNCATED AT 250 WORDS)