Developmental regulation of expression of renal potassium secretory channels

Purpose 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 s/o, 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.