Kcnq1 contributes to an adrenergic-sensitive steady-state K+ current in mouse heart
Abbreviated Journal Title
Biochem. Biophys. Res. Commun.
potassium channel; transgenic mouse; electrophysiology; adrenergic; heart; LANGE-NIELSEN-SYNDROME; POTASSIUM CHANNEL; VENTRICULAR MYOCYTES; TARGETED DISRUPTION; RAT-HEART; EXPRESSION; MICE; PROTEINS; SUBUNIT; KVLQT1; Biochemistry & Molecular Biology; Biophysics
It has been suggested that Kcnel subunits are required for adrenergic regulation of Kcnq1 potassium channels. However, in adult mouse hearts, which do not express Kcne1, loss of Kcnq1 causes a Long QT phenotype during adrenergic challenge, raising the possibility that native Kcnq1 currents exist and are adrenergically regulated even in absence of Kcnel. Here, we used immunoblotting and immunohistochemical staining to show that Kcnq1 protein is present in adult mouse hearts. Voltage-clamp experiments demonstrated that Kcnq1 contributes to a steady-state outward current (I-SS) in wild-type (Kcnq1+/+) ventricular myocytes during isoproterenol stimulation, resulting in a significant 7.1% increase in Iss density (0.43 +/- 0.16 pA/pF, p < 0.05, n = 15), an effect that was absent in Kcnq1-deficient (Kcnq1(-/-)) myocytes (-0.14 +/- 0.13 pA/pF, n = 17). These results demonstrate for the first time that Kcnq1 protein is expressed in adult mouse hearts where it contributes to a beta-adrenergic-induced component of Iss that does not require co-assembly with Kcnel. (c) 2007 Elsevier Inc. All rights reserved.
Biochemical and Biophysical Research Communications
"Kcnq1 contributes to an adrenergic-sensitive steady-state K+ current in mouse heart" (2007). Faculty Bibliography 2000s. 7310.