β₁-Adrenoceptor Autoantibodies Affect Action Potential Duration and Delayed Rectifier Potassium Currents in Guinea Pigs

β₁-Adrenoceptor autoantibodies (β₁-AAs) affect the action potential duration (APD) in cardiomyocytes and are related to ventricular arrhythmias. The delayed rectifier potassium current (I _K) plays a crucial role in APD, but the effects of β₁-AAs on I _K have not been completely illuminated. This work aimed to observe the effects of β₁-AAs on I _K and APD and further explore the mechanisms of β₁-AA-mediated ventricular arrhythmias. β₁-AAs were obtained from sera of patients with coronary heart disease (CHD) and nonsustained ventricular tachycardia. With whole-cell patch clamp technique, action potentials and I _K were recorded. The results illustrated 0.1 μmol/L β₁-AAs shortened APD at 50 % (APD₅₀) and 90 % (APD₉₀) of the repolarization. However, at 0.01 μmol/L, β₁-AAs had no effects on either APD₉₀ or APD₅₀ (P > 0.05). At 0.001 μmol/L, β₁-AAs significantly prolonged APD₉₀ and APD₅₀. Moreover, β₁-AAs (0.001, 0.01, 0.1 μmol/L) dose-dependently increased the rapidly activating delayed rectifier potassium current (I _Kr), but similarly decreased the slowly activating delayed rectifier potassium current (I _Ks) and increased L-type calcium currents at the different concentrations. Taken together, the IKr increase induced by high β1-AA concentrations is responsible for a significant APD reduction which would contribute to repolarization changes and trigger the malignant ventricular arrhythmias in CHD patients.