Regional localization of renal Na(+)-H+ antiporter: response to respiratory acidosis

The Na(+)-H+ antiporter of renal brush-border membranes has been well characterized and plays a role in adaptation to acidosis. Na(+)-H+ antiporter activity has been described in other renal regions, but its kinetics as well as its role in adaptation to acidosis are unclear. Thus we measured Na(+)-H+ antiporter activity in membrane vesicles of outer and inner stripes of outer medulla (OSOM and ISOM, respectively) and in plasma membranes from papilla and compared it to Na(+)-H+ antiporter activity of the cortex in control and hypercapnic rabbits. Chronic hypercapnia (induced by exposure to CO2 for 48 h) was associated with significantly higher PCO2 and plasma HCO3- and lower urine pH than controls. In control animals, magnitude of Vmax of amiloride-sensitive component of Na(+)-H+ antiporter (expressed as fluorescence units.300 micrograms protein-1.min-1) was 392.2 +/- 32 in cortex, 115 +/- 9.7 in OSOM, 66.1 +/- 9.4 in 15-25% (F1) fraction and 118.7 +/- 16.8 in 25-40% (F2) fraction of ISOM, respectively, and 79.3 +/- 5.2 in papilla. These values were significantly different from each other except between F1 and papilla and F2 and OSOM. The Km for Na, however, was not different, suggesting that the renal Na(+)-H+ antiporter is basically the same in different renal regions but displays different activity. Hypercapnia for 48 h increased significantly the amiloride-sensitive component of Na(+)-H+ antiporter by 60% in cortex, 43% in F1, and 29% in papilla but failed to alter Vmax in OSOM.(ABSTRACT TRUNCATED AT 250 WORDS)