title: Effect of aldosterone on BK channel expression in mammalian cortical collecting duct.
abstract: Apical large-conductance Ca(2+)-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 approximately 1 to 5 nl.min(-1).mm(-1), the increase in J(Na) was greater in LS vs. HS rabbits, yet the flow-stimulated increase in J(K) 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.
authors.affiliation: Division of Pediatric Nephrology, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA.
authors.forename: Genevieve
authors.initials: G
authors.lastname: Estilo
authors.forename: Wen
authors.initials: W
authors.lastname: Liu
authors.forename: Nuria
authors.initials: N
authors.lastname: Pastor-Soler
authors.forename: Phillip
authors.initials: P
authors.lastname: Mitchell
authors.forename: Marcelo D
authors.initials: MD
authors.lastname: Carattino
authors.forename: Thomas R
authors.initials: TR
authors.lastname: Kleyman
authors.forename: Lisa M
authors.initials: LM
authors.lastname: Satlin
mesh_terms: D000450:Aldosterone / Q000097:blood / Q000378:metabolism*; D000818:Animals; D002412:Cations / Q000378:metabolism; D004573:Electrolytes / Q000097:blood / Q000652:urine; D007150:Immunohistochemistry; D066298:In Vitro Techniques; D007685:Kidney Tubules, Collecting / Q000378:metabolism*; D051036:Large-Conductance Calcium-Activated Potassium Channels / Q000378:metabolism*; D017419:Potassium, Dietary / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D011817:Rabbits; D012982:Sodium, Dietary / Q000378:metabolism*
chemical_list: D002412:Cations; D004573:Electrolytes; D051036:Large-Conductance Calcium-Activated Potassium Channels; D017419:Potassium, Dietary; D012333:RNA, Messenger; D012982:Sodium, Dietary; D000450:Aldosterone