Regulation of potassium transport in the maturing kidney

Kidneys of full-term newborn humans and animals conserve potassium (K+), a condition essential for growth. The cortical collecting duct (CCD) is uniquely adapted to accomplish this task early in life. CCDs isolated from newborn rabbits and microperfused in vitro show no net K+ secretion until after the third week of life; in contrast, segments isolated from adult animals secrete net K+ at high rates. The magnitude and direction of net K+ transport in the CCD reflect the balance of opposing fluxes of K+ secretion and K+ absorption mediated by principal and intercalated cells, respectively. The absence of net K+ secretion in the CCD early in life may thus be caused by a limited capacity of principal cells for K+ secretion and/or an excess of K+ absorption by intercalated cells. Recent studies provide data to support both possibilities. Patch-clamp analysis detects few conducting apical K+-secretory channels in neonatal principal cells, whereas fluorescent functional assays identify significant activity of the apical hydrogen, potassium adenosine triphosphatase (H+,K+-ATPase), a pump that reabsorbs K+ in exchange for H+s, in adjacent intercalated cells. Under conditions prevailing in vivo, the sum of the fluxes mediated by these two cell types likely contributes to the relative K+ retention characteristic of the neonatal kidney.