The role of cortical Na,K-ATPase in distal nephron potassium secretion by the immature canine kidney.

Amiloride-sensitive potassium secretion in response to acute potassium loading is lower in the newborn than in the adult. Potassium secretion is a function of late distal tubule and cortical collecting tubule Na,K-ATPase activity. Na,K-ATPase activity in vivo is determined by enzyme abundance and catalytic turnover. Chronic potassium supplementation increases potassium secretory capacity in the adult by increasing enzyme abundance in the late distal and cortical collecting tubules. We hypothesized that the lower potassium secretory capacity of the newborn was the result of lower late distal and cortical collecting tubule Na,K-ATPase activity and could be similarly enhanced. To test this hypothesis, newborn dogs were supplemented with 6 mmol KCl.d-1.kg-1 for 1 wk; age-matched litter mate controls were not (n = 8 pairs). Potassium supplementation resulted in a mean increase in Vmax Na,K-ATPase activity in vitro (proportional to pump abundance) of 70 +/- 42%. Mean Na,K-ATPase activities +/- SEM were 279 +/- 58 versus 198 +/- 44 nmol inorganic P. h-1.microgram DNA-1, p = 0.05. However, amiloride-sensitive potassium secretion after an acute potassium load of 20 mumol.min-1.kg-1 over 150 min was not enhanced (9.6 +/- 1.8 versus 8.9 +/- 0.8 mumol.min-1.kg-1, potassium-supplemented versus control animals). We conclude that lower enzyme abundance is not primarily responsible for the newborn's lower potassium secretory capacity. We speculate that the factor that limits secretion in the newborn during acute potassium loading does so by restricting catalytic turnover of the enzyme in vivo.