NFATc3 Regulates Kv2.1 Expression in Arterial Smooth Muscle

摘要: Voltage-gated K+ (Kv) channels control the excitability of arterial smooth muscle. However, molecular mechanisms regulating Kv channel function in muscle remain unclear. We examined hypothesis that vasoactive peptide angiotensin II (Ang II) regulates via calcineurin-dependent activation transcription factor NFAT. found sustained administration Ang decreased currents (IKv) by reducing expression Kv2.1 subunits. This effect was independent pressure but required Ca2+ influx through L-type channels. Consistent with our hypothesis, we calcineurin and NFATc3 are obligatory components signaling cascade mediating reduced IKv II. conclude exposure increases Ca2+, which leads to NFATc3, culminating function. These results support novel concept controls expression.