Effect of aldosterone on BK channel expression in mammalian cortical collecting duct

Apical large-conductance Ca2+-activated K+ (BK) channels in the cortical collecting duct (CCD) mediate flow-stimulated K+ secretion. Dietary K+ loading for 10-14 days 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 F, Zhou H, Morimoto T, Bruns JB, Li HS, Liu W, Kleyman TR, Satlin LM. Am J Physiol Renal Physiol 289: F922-F932, 2005). To test whether this adaptation was mediated by a K+-induced increase in aldosterone, New Zealand White rabbits were fed a low-Na+ (LS) or high-Na+ (HS) diet for 7-10 days to alter circulating levels of aldosterone but not serum K+ concentration. Single CCDs were isolated for quantitation of BK channel subunit (total, alpha-splice variants, beta-isoforms) mRNA abundance by real-time PCR and measurement of net transepithelial Na+ (J(Na)) and K+ (J(K)) transport by microperfusion; kidneys were processed for immunolocalization of BK alpha-subunit by immunofluorescence microscopy. At the time of death, LS rabbits excreted no urinary Na+ and had higher circulating levels of aldosterone than HS animals. The relative abundance of BK alpha-, beta(2)-, and beta(4)-subunit mRNA and localization of immunodetectable alpha-subunit were similar in CCDs from LS and HS animals. In response to an increase in tubular flow rate from similar to 1 to 5 nl.min(-1).mm(-1), the increase in JNa was 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.