Developmental regulation of expression of renal potassium secretory channels

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.

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 Ca 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.

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.