Apical BK channels in the CCD mediate flow-stimulated K secretion. Dietary K loading for 10-14 d leads to an increase in BK channel mRNA abundance, enhanced flow-stimulated K secretion in microperfused CCDs, and a redistribution of immunodetectable channels from an intracellular pool to the apical membrane (Najjar et al, AJP Renal 289:F922, 2005). To test whether this adaptation was mediated by a K-induced increase in aldosterone, NZW rabbits were fed a low (LS) or high (HS) Na diet for 7-10 d to alter circulating levels of aldosterone but not serum K concentration. Single CCDs were isolated for quantitation of BK channel subunit (total, splice variants, isoforms) mRNA abundance by real-time PCR and measurement of net transepithelial Na (JNa) and K (JK) transport by microperfusion; kidneys were processed for immunolocalization of BK subunit by immunofluorescence microscopy. At the time of sacrifice, LS rabbits excreted no urinary Na and had higher circulating levels of aldosterone than did HS animals. The relative abundance of BK , 2, and 4-subunit mRNA and localization of immunodetectable subunit were similar in CCDs from LS and HS animals. In response to an increase in tubular flow rate from 1 to 5 nl/min per mm, the increase in JNa tended to be greater in LS vs. HS rabbits, yet the flow-stimulated increase in JK was similar in both groups. These data suggest that aldosterone does not contribute to the regulation of BK channel expression/activity in response to dietary K loading.