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The cortical collecting duct (CCD) plays a key role in regulated [K.sup.+] secretion, which is mediated mainly through renal outer medullary [K.sup.+] (ROMK) channels located in the apical membrane. However, the mechanisms of the regulation of urinary [K.sup.+] excretion with regard to [K.sup.+] balance are not well known. We took advantage of a recently established mouse CCD cell line (mCC[D.sub.c11]) to investigate the regulation of [K.sup.+] secretion by mineralocorticoid and [K.sup.+] concentration. We show that this cell line expresses ROMK mRNA and a barium-sensitive [K.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.sup.+] conductance, while it increased the amiloride-sensitive [Na.sup.+] transport. Overnight exposure to a high [K.sup.+] (7 mM) concentration produced a small but significant increase in the apical membrane barium-sensitive [K.sup.+] conductance. The mRNA levels of all ROMK isoforms measured by qRT-PCR were not changed by altering the basolateral [K.sup.+] concentration but were decreased by 15-45% 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.sup.+] loss which would otherwise result from the increased electrogenic [Na.sup.+] transport and associated depolarization of the apical membrane in the CCD. In conclusion, mCC[D.sub.c11] cells demonstrate a significant [K.sup.+] secretion, probably mediated by ROMK, which is not stimulated by aldosterone but increased by overnight exposure to a high [K.sup.+] concentration. cultured mCCD cells; urinary potassium excretion; aldosterone

(14C)urate and p-(14C)aminohippurate (PAH) transport is linked to sodium transport through indirect coupling between sodium-alpha-ketoglutarate cotransport and PAH/alpha ketoglutarate exchanger in human brush border membrane (BBM) vesicles. The human BBM most likely contains two anion exchangers for urate and one for PAH. The decrease in urate excretion is associated with the stimulation of urate reabsorption by pyrazinoate. In humans, only 10% of the filtered load of urate is excreted in urine under normal physiological conditions.

Analysis of the process of urate transport in human renal brush-border membrane (BBM) residues reveals that anion exchanger plays a significant role in urate reabsorption in humans. The human exchanger exhibits a low affinity for OH- and P-aminohippurate. A voltage-dependent process is also involved in the transport of urate in human BBM.

The cortical collecting duct (CCD) plays a key role in regulated K+ secretion, which is mediated mainly through renal outer medullary K+ (ROMK) channels located in the apical membrane. However, the mechanisms of the regulation of urinary K+ excretion with regard to K+ balance are not well known. We took advantage of a recently established mouse CCD cell line (mCCDc11) to investigate the regulation of K+ secretion by mineralocorticoid and K+ concentration. We show that this cell line expresses ROMK mRNA and a barium-sensitive K+ conductance in its apical membrane. As this conductance is sensitive to tertiapin-Q, with an apparent affinity of 6 nM, and to intracelIular acidification, it is probably mediated by ROMK. Overnight exposure to 100 nM aldosterone did not significantly change the K+ conductance, while it increased the amiloride-sensitive Na+ transport. Overnight exposure to a high K+ (7 mM) concentration produced a small but significant increase in the apical membrane barium-sensitive K+ conductance. The mRNA levels of all ROMK isoforms measured by qRT-PCR were not changed by altering the basolateral K+ concentration but were decreased by 15-45% 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+ loss which would otherwise result from the increased electrogenic Na+ transport and associated depolarization of the apical membrane in the CCD. In conclusion, mCCDc11 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. [ABSTRACT FROM AUTHOR]