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

Abstract

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, α-splice variants, β-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 α-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 α-, β₂-, and β₄-subunit mRNA and localization of immunodetectable α-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⁻¹·mm⁻¹, the increase in J_Nawas greater in LS vs. HS rabbits, yet the flow-stimulated increase in J_Kwas 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.