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Intact colonic K C a 1.1 channel activity in KCNMB2 knockout mice.

Mammalian potassium homeostasis results from tightly regulated renal and colonic excretion, which balances the unregulated dietary K+ intake. Colonic K+ secretion follows the pump-leak model, in which the large conductance Ca2+ -activated K+ channel (KC a 1.1 ) is well established as the sole, but highly regulated apical K+ conductance. The physiological importance of auxiliary β and γ subunits of the pore-forming α -subunit of the KC a 1.1 channel is not yet fully established. This study investigates colonic K+ secretion in a global knockout mouse of the KC a 1.1- β 2-subunit (KCNMB2-/- ), which apparently is the only β -subunit of the colonic enterocyte KC a 1.1 channel. We can report that: (1) Neither KC a 1.1 α - nor the remaining β -subunits were compensatory transcriptional regulated in colonic epithelia of KCNMB2-/- mice. (2) Colonic epithelia from KCNMB2-/- mice displayed equal basal and ATP-induced KC a 1.1-mediated K+ conductance as compared to KCNMB2+/+ (3) K+ secretion was increased in KCNMB2-/- epithelia compared to wild-type epithelia from animals fed an aldosterone-inducing diet. (4) Importantly, the apical K+ conductance was abolished by the specific blocker of KC a 1.1 channel iberiotoxin in both KCNMB2+/+ and KCNMB2-/- mice. Recently a novel family of auxiliary γ -subunits of the KC a 1.1 channel has been described. (5) We detected the γ 1-subunit (LRRC26) mRNA in colonic epithelia. To investigate the physiological role of the γ 1-subunit of KC a 1.1 channels in colonic K+ secretion, we acquired an LRRC26 knockout mouse. (6) Unexpectedly, LRRC26 mice had a perinatal lethal phenotype, thus preventing functional measurements. On this basis we conclude that colonic K+ secretion is intact or even increased in mice lacking the β 2-subunit of KC a 1.1 channel complex despite no additional compensatory induction of KC a 1.1 β -subunits.

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