AbstractPurpose of review
Somatic growth is associated with an increase in total body K+ content. K+ homeostasis is regulated, in large part, by urinary K+ excretion. Within the adult kidney and specifically the cortical collecting duct, K+ secretion is accomplished by the passive diffusion of cell K+ into the urinary fluid down a favorable electrochemical gradient through K+ selective channels. The purpose of this review is to summarize the results of recent studies that provide insight into how the cortical collecting duct is uniquely adapted for K+ retention early in life.Recent findings
Electrophysiological analyses have identified two types of apical K+ channels in the mammalian cortical collecting duct. The prevalence of the secretory K+ channel and its high open probability at the resting membrane potential in the adult has led to the belief that this channel mediates baseline K+ secretion. The Ca2+ and stretch-activated maxi-K channel has been proposed to mediate flow-stimulated K+ secretion. In contrast to the high rates of K+ secretion observed in adult cortical collecting ducts microperfused in vitro, segments isolated from neonatal animals show no significant net K+ transport until after the third week of postnatal life. The temporal delay between expression of conducting secretory K+ channels (baseline K+ secretion) and maxi-K channels (flow-stimulated K+ secretion) in the maturing cortical collecting duct reflect unique developmental programs regulating the transcription and/or translation of ROMK (rat outer medullary K channel) and slo, the molecular correlates of the secretory K+ and maxi-K channels, respectively.Summary
The K+ retention characteristic of the neonatal kidney is due, in part, to a paucity of distinct K+ channels mediating baseline and flow-stimulated K+ secretion in the collecting duct. The signals directing the developmental regulation of channel expression are as yet unknown.