ROMK is expressed in the urinary tract at both protein and mRNA levels. Significant enlargement and hypertrophy of the bladder may contribute to hydronephrosis in male ROMK KO mice.
THGP modulation of ROMK function confers a new role of THGP on renal ion transport and may contribute to salt wasting observed in FJHN/MCKD-2/GCKD patients.
We propose that in taste buds ROMK in type I/glial-like cells may serve a homeostatic function excreting excess K(+) through the apical pore and allowing excitable taste cells to maintain a hyperpolarized resting membrane potential.
cortical collecting duct cells demonstrate a significant K(+) secretion probably mediated by ROMK which is not stimulated by aldosterone but increased by overnight exposure to a high K(+) concentration
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