%0 Journal Article
%T Intact colonic KC
a1.1 channel activity in KCNMB2 knockout mice
%A Casper K. Larsen
%A Helle A. Praetorius
%A Jens Leipziger
%A Mads V. Sorensen
%J Archive of "Physiological Reports".
%D 2017
%R 10.14814/phy2.13179
%X Mammalian potassium homeostasis results from tightly regulated renal and colonic excretion, which balances the unregulated dietary K+ intake. Colonic K+ secretion follows the pump坼leak model, in which the large conductance Ca2+坼activated K+ channel (KC a1.1) is well established as the sole, but highly regulated apical K+ conductance. The physiological importance of auxiliary 汕 and 污 subunits of the pore坼forming 汐坼subunit of the KC a1.1 channel is not yet fully established. This study investigates colonic K+ secretion in a global knockout mouse of the KC a1.1坼汕2坼subunit (KCNMB2ˋ/ˋ), which apparently is the only 汕坼subunit of the colonic enterocyte KC a1.1 channel. We can report that: (1) Neither KC a1.1 汐坼 nor the remaining 汕坼subunits were compensatory transcriptional regulated in colonic epithelia of KCNMB2ˋ/ˋ mice. (2) Colonic epithelia from KCNMB2ˋ/ˋ mice displayed equal basal and ATP坼induced KC a1.1坼mediated K+ conductance as compared to KCNMB2+/+. (3) K+ secretion was increased in KCNMB2ˋ/ˋ epithelia compared to wild坼type epithelia from animals fed an aldosterone坼inducing diet. (4) Importantly, the apical K+ conductance was abolished by the specific blocker of KC a1.1 channel iberiotoxin in both KCNMB2+/+ and KCNMB2ˋ/ˋ mice. Recently a novel family of auxiliary 污坼subunits of the KC a1.1 channel has been described. (5) We detected the 污1坼subunit (LRRC26) mRNA in colonic epithelia. To investigate the physiological role of the 污1坼subunit of KC a1.1 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 汕2坼subunit of KC a1.1 channel complex despite no additional compensatory induction of KC a1.1 汕坼subunits
%K BK channel
%K K+ Homeostasis
%K K+ secretion
%K KCa1.1
%K KCa1.1 beta2 subunit
%K LRCC26
%K Maxi K+ channel
%U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5350182/