ROMK

ROMK stands for renal outer medullary potassium channel, an inwardly rectifying potassium (Kir) channel of the Kir1.x subfamily. The channel is encoded by the KCNJ1 gene in humans and forms potassium-permeable channels that contribute to renal potassium handling.

In the kidney, ROMK is expressed mainly in the thick ascending limb of the loop of Henle and in the collecting duct, where it localizes to the apical membrane of tubular cells. Through these apical channels, ROMK participates in potassium secretion into the tubular lumen and in potassium recycling that is necessary for the activity of the NKCC2 transporter in the thick ascending limb.

ROMK activity is regulated by cellular energy state and hormonal signaling. It is inhibited by intracellular ATP and polyamines and can be influenced by flow-dependent stimuli; aldosterone increases ROMK expression in the collecting duct, promoting potassium secretion. The channel is sensitive to pharmacological blockers such as barium and is an integral part of the broader regulatory network that maintains electrolyte balance and blood pressure.

Clinical significance: Mutations in KCNJ1, the gene encoding ROMK, cause antenatal Bartter syndrome type 2. This disorder of salt handling presents in infancy with polyuria, hypokalemia, metabolic alkalosis, and growth retardation, reflecting impaired potassium recycling in the thick ascending limb and reduced NKCC2 function.

ROMK is a key component of renal potassium homeostasis and a well-studied model for inwardly rectifying potassium channels in the Kir family.