Regulation of the ROMK potassium channel in the kidney.

Abstract

ROMK is a gene encoding inwardly rectifying adenosine triphosphate regulated K+ channels. Alternative splicing of ROMK exons yields several different transcripts, ROMK 1-3, that are differentially expressed along the nephron. Cloned ROMK channels expressed in Xenopus oocytes exhibit properties similar to those of the native low-conductance K+ secretory channels in cortical collecting duct and medullary thick ascending limb, as manifested by use of the patch-clamp technique. These similarities between the cloned and native channels suggest that ROMK represents the low-conductance secretory K+ channels in the kidney. We studied the role of dietary K+ and aldosterone in the regulation of ROMK mRNA expression in the rat kidney. K+ deficiency downregulated ROMK mRNA in cortex and medulla. Adrenalectomy markedly downregulated cortical ROMK, while it increased it in the medulla. In adrenalectomized rats K+ deficiency decreased ROMK mRNA in cortex and medulla similarly to intact rats. Na-K-ATPase subunits alpha1 and beta1 were regulated in parallel to the regulation of ROMK. In the medulla ROMK mRNA correlated highly with serum K+ and with the alpha1 and beta1 subunits of Na-K-ATPase. These results show that cortical ROMK expression is regulated by aldosterone and K+, while the medullary ROMK mRNA is regulated by serum K+, irrespective of aldosterone.