The Effect Of Angiotensin Ⅱ On The Expression Of Kv4.2 Potassium Channel And Its Underlying Mechanism In Neonatal Rat Cardiomyocytes

The arrhythmia is the common complication for cardiac hypertrophy and failure. The mortality of heart failure is still very high due to sudden cardiac death. Therefore, exploring the electrophysiological mechanism of arrhythmias and find the effiective anti-arrhymia drug are the major issues in the field of cardiovascular research. The studies have showed that the most significant change of electrophysiology is the prolongation of action potential duration in the cardiac hypertrophy and failure. The transient outward potassium current (Ito) is downregulated in hypertrophied and failing heart from experimental animals and patients with heart failure. Ito is the key repolarizing current in the early phase of membrane action potential and the down-regulation of Ito current density prolong the time course of the action potential.Among all of the neuronal or hormonal factors that cause the load-induced cardiac hypertrophy the angiotensin II (Ang II) is the most important hormone. Many experiments indicate that Ang II play a key role in the course of cardiac hypertrophy. It is reported that Ang II downregulates Kv4.3 protein expression and reduced the Ito in cardiac myocytes. Some studies show...