{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T20:46:27Z","timestamp":1778273187726,"version":"3.51.4"},"reference-count":40,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2009,5]]},"abstract":"<jats:p>The cortical collecting duct (CCD) plays a key role in regulated K<jats:sup>+<\/jats:sup>secretion, which is mediated mainly through renal outer medullary K<jats:sup>+<\/jats:sup>(ROMK) channels located in the apical membrane. However, the mechanisms of the regulation of urinary K<jats:sup>+<\/jats:sup>excretion with regard to K<jats:sup>+<\/jats:sup>balance are not well known. We took advantage of a recently established mouse CCD cell line (mCCD<jats:sub>cl1<\/jats:sub>) to investigate the regulation of K<jats:sup>+<\/jats:sup>secretion by mineralocorticoid and K<jats:sup>+<\/jats:sup>concentration. We show that this cell line expresses ROMK mRNA and a barium-sensitive K<jats:sup>+<\/jats:sup>conductance in its apical membrane. As this conductance is sensitive to tertiapin-Q, with an apparent affinity of 6 nM, and to intracellular acidification, it is probably mediated by ROMK. Overnight exposure to 100 nM aldosterone did not significantly change the K<jats:sup>+<\/jats:sup>conductance, while it increased the amiloride-sensitive Na<jats:sup>+<\/jats:sup>transport. Overnight exposure to a high K<jats:sup>+<\/jats:sup>(7 mM) concentration produced a small but significant increase in the apical membrane barium-sensitive K<jats:sup>+<\/jats:sup>conductance. The mRNA levels of all ROMK isoforms measured by qRT-PCR were not changed by altering the basolateral K<jats:sup>+<\/jats:sup>concentration but were decreased by 15\u201345% upon treatment with aldosterone (0.3 or 300 nM for 1 and 3 h). The paradoxical response of ROMK expression to aldosterone could possibly work as a preventative mechanism to avoid excessive K<jats:sup>+<\/jats:sup>loss which would otherwise result from the increased electrogenic Na<jats:sup>+<\/jats:sup>transport and associated depolarization of the apical membrane in the CCD. In conclusion, mCCD<jats:sub>cl1<\/jats:sub>cells demonstrate a significant K<jats:sup>+<\/jats:sup>secretion, probably mediated by ROMK, which is not stimulated by aldosterone but increased by overnight exposure to a high K<jats:sup>+<\/jats:sup>concentration.<\/jats:p>","DOI":"10.1152\/ajprenal.90475.2008","type":"journal-article","created":{"date-parts":[[2009,3,19]],"date-time":"2009-03-19T00:55:14Z","timestamp":1237424114000},"page":"F966-F975","source":"Crossref","is-referenced-by-count":27,"title":["Effects of mineralocorticoid and K<sup>+<\/sup>concentration on K<sup>+<\/sup>secretion and ROMK channel expression in a mouse cortical collecting duct cell 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