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• W2045646421 abstract "To the Editor: A recent publication by Bailey et al.1.Bailey M.A. Cantone A. Yan Q. et al.Maxi-K channels contribute to urinary potassium excretion in the ROMK-deficient mouse model of Type II Bartter's syndrome and in adaptation to a high-K diet.Kidney Int. 2006; 70: 51-59Abstract Full Text Full Text PDF PubMed Scopus (133) Google Scholar resurrected the micropuncture technique to address a long-standing question regarding the ion channels responsible for K+ secretion in the distal nephron. In this study, the investigators demonstrated that the large, Ca2+-activated K+ channel (maxi K+) has an important role to secrete K+ when demand is high. The history of the maxi K+ (now genetically termed slowpoke or slo) as a renal K+ secretory channel began in 1984 when the maxi K+ in the rabbit cortical collecting duct was the first renal epithelial channel described at the single channel level by the patch-clamp technique.2.Hunter M. Lopes A.G. Boulpaep E.L. et al.Single channel recordings of calcium-activated potassium channels in the apical membrane of rabbit cortical collecting tubules.Proc Natl Acad Sci. 1984; 81: 4237-4239Crossref PubMed Scopus (128) Google Scholar However, the maxi K+ was soon discarded as a K+ secretory channel because of its low open probability at physiological intracellular Ca2+ concentrations and membrane potentials. The maxi K+ gave way to a small conductance K+ channel (SK), open 80% of the time in physiological conditions.3.Frindt G. Palmer L.G. Low-conductance K channels in apical membrane of rat cortical collecting tubule.Am J Physiol. 1989; 256: F143-F151PubMed Google Scholar The maxi K+ reemerged as a secretory channel on discovering that high flow activated maxi K+ of isolated rabbit connecting tubules (CNTs)4.Taniguchi J. Imai M. Flow-dependent activation of maxi K+ channels in apical membrane of rabbit connecting tubule.J Membr Biol. 1998; 164: 35-45Crossref PubMed Scopus (85) Google Scholar and collecting ducts.5.Woda C.B. Bragin A. Kleyman T.R. Satlin L.M. Flow-dependent K+ secretion in the cortical collecting duct is mediated by a maxi-K channel.Am J Physiol Renal Physiol. 2001; 280: F786-F793PubMed Google Scholar A subsequent in vivo study showed that flow-mediated K+ secretion was absent when an accessory subunit of the maxi K+ was genetically deleted.6.Pluznick J.L. Wei P. Grimm P.R. Sansom S.C. BK-{beta}1 subunit: immunolocalization in the mammalian connecting tubule and its role in the kaliure.Am J Physiol Renal Physiol. 2005; 288: F846-F854Crossref PubMed Scopus (81) Google Scholar The Bailey et al.1.Bailey M.A. Cantone A. Yan Q. et al.Maxi-K channels contribute to urinary potassium excretion in the ROMK-deficient mouse model of Type II Bartter's syndrome and in adaptation to a high-K diet.Kidney Int. 2006; 70: 51-59Abstract Full Text Full Text PDF PubMed Scopus (133) Google Scholar study is the first micropuncture study to provide evidence for the maxi K+ as a secretory channel in the distal nephron of the mouse. The first cloning of a renal K+ channel was from the inner stripe of the rat outer medulla (ROMK). ROMK, classified as part of the inward rectifying family of K+ channels (KIR1.1), is the equivalent of SK.7.Ho K. Nichols C.G. Lederer W.J. et al.1oning and expression of an inwardly rectifying ATP-regulated potassium channel.Nature. 1993; 362: 31-38Crossref PubMed Scopus (807) Google Scholar The in vivo significance of ROMK was demonstrated after developing the ROMK−/− mouse.8.Lorenz J.N. Baird N.R. Judd L.M. et al.Impaired renal NaCl absorption in mice lacking the ROMK potassium channel, a model for type II Bartter's syndrome.J Biol Chem. 2002; 277: 37871-37880Crossref PubMed Scopus (146) Google Scholar Patch clamping confirmed that SK was absent in the thick ascending limb (TAL) and cortical collecting duct of ROMK−/−.9.Lu M. Wang T. Yan Q. et al.Absence of small conductance K+ channel (SK) activity in apical membranes of thick ascending limb and cortical collecting duct in ROMK (Bartter's) knockout mice.J Biol Chem. 2002; 277: 37881-37887Crossref PubMed Scopus (145) Google Scholar However, instead of a K+ secretory defect, it was surprising that excretion of K+ in the ROMK−/− mouse was increased. Bailey et al. offered two explanations for the K+ loss in ROMK−/−. First, without ROMK, an absence of K+ recycling in the apical membrane of the TAL results in increased distal flow, which activates maxi K+ in distal segments. Second, the absence of ROMK in the TAL resulted in reduced K+ reabsorption in the TAL. The combination of recycling K+ via ROMK and a Na+-selective tight junction creates an efficiently maximized Na+ reabsorption in the TAL (see Figure 1a). In the absence of K+ recycling, the large decrease in Na+ and Cl− reabsorption in the TAL results in a large quantity of Na+, Cl− and fluid delivered to the distal neprhon. Thus, the first explanation is consistent with the participation of maxi K+ in flow-induced K secretion. However, the second explanation for increased K+ excretion in ROMK−/−, namely that the absence of ROMK resulted in reduced K+ reabsorption in the TAL, is problematic in my opinion. This explanation was offered because the K+ concentration in the earliest micropunctured portion of the distal tubule was higher than in the TAL. On this point, I disagree with Bailey et al. Rather, I believe that there must be another explanation for the increased [K+]i in the distal tubule. In my view, K+ secretion by other distal transporters or channels, including the maxi K+, is responsible for the entire urinary loss of K+ in ROMK−/−. When the transporters of the TAL are modeled in wild type (Figure 1a) and ROMK−/− (Figure 1b), it is clear that K+ reabsorption can continue in the TAL in the absence of ROMK. By inhibiting the NaK2Cl, furosemide would eliminate all Na+, K+, and Cl− transport in the TAL (Figure 1c). Eliminating ROMK will remove an electrogenic component of NaCl reabsorption that is dependent on K+ recycling in the TAL. However electroneural K+ reabsorption is independent of ROMK. As long as K+ is delivered to the TAL from upstream segments, K+ reabsorption will continue. Indeed, experimentally blocking ROMK with barium inhibited NaCl transport without affecting net K+ transport.10.Walter S.J. Shirley D.G. Folkerd E.J. Unwin R.J. Effects of the potassium channel blocker barium on sodium and potassium transport in the rat loop of Henle in vivo.Exp Physiol. 2001; 86: 469-474Crossref PubMed Scopus (15) Google Scholar The additional K+ measured in the distal convoluted tubule (DCT) of ROMK−/− by Bailey et al. may have been due to K+ secretion in a later portion of the distal tubule (DCT2). In the rabbit kidney, epithelial sodium channel (ENaC) and maxi K+ are distinctly localized together in the connecting tubule. However, in the mouse kidney, there is considerable overlap with ENaC in the DCT2,6.Pluznick J.L. Wei P. Grimm P.R. Sansom S.C. BK-{beta}1 subunit: immunolocalization in the mammalian connecting tubule and its role in the kaliure.Am J Physiol Renal Physiol. 2005; 288: F846-F854Crossref PubMed Scopus (81) Google Scholar,11.Biner H.L. Arpin-Bott M.P. Loffing J. et al.Human cortical distal nephron: distribution of electrolyte and water transport pathways.J Am Soc Nephrol. 2002; 13: 836-847PubMed Google Scholar leaving a very short DCT1 available for micropuncture. The increased negative potential in the micropunctured segment of ROMK−/− is evidence that the microelectrode was placed in the ENaC-associated DCT2. The presence of ENaC would give a driving force for K+ secretion by maxi K+, which may have enhanced expression in the DCT2 of ROMK−/−. An explanation by Bailey et al. for a possible decrease in K+ reabsorption in the TAL is that [Cl−]i would increase in the TAL with the loss of ROMK (Figure 6 of Bailey et al.). High [Cl−]i could feedback to inhibit NaK2Cl. The [Cl−] has not been measured in the TAL of ROMK−/−. However, in the rabbit TAL, [Cl−]i has been measured at 54 mM,12.Salomonsson M. Gonzalez E. Westerlund P. Persson A.E. Chloride concentration in macula densa and cortical thick ascending limb cells.Kidney Int Suppl. 1991; 32: S51-S54PubMed Google Scholar yielding an equilibrium potential of -25 mV (140 mM Cl− outside). With a membrane potential of -70 mV, there is a large driving force for Cl− transport across the basolateral membrane. Without the apical K+ conductance in ROMK−/−, the basolateral membrane potential will depolarize to between -30 and -40 mV as the cellular conductance is now dominated by the basolateral Cl− conductance. However, unless the ionic transport via Na–K–2Cl is increased, [Cl−]i would not increase in the absence of ROMK. Not withstanding the argument that K+ absorption is impaired in the TAL of ROMK−/−, the study by Bailey et al. was a monumental tour de force and a ‘back to the future’ study for two reasons. First, the formerly abandoned micropuncture technique was used as a means to determine the in vivo roles of K+ channels in the distal nephron and second, in the process, the initially abandoned maxi K+ was revived as a physiological secretory channel for K+ in the distal nephron." @default.
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