Abstract:

Objective    To investigate the influences of the adrenoceptor β₁ antibody (anti-ADRβ1, simulating autoantibody) on potassium channels. Methods    Mouse ventricular cardiac myocytes were prepared by enzymatic isolating technique. The whole-cell patch-clamp technique was used to record K+ currents, in which signals were amplified with an HEKA EPC-10 patch clamp amplifier and controlled by Pulse software. The voltage protocol was a one-second depolarizing pulse from -50 to +50mV in 10mV increments and at a holding potential of -60mV. Cells were perfused with normal bath solution for 10 minutes to stabilize the currents, and then were perfused with anti-ADRβ₁ in different concentrations (1/500, 1/100 or 1/50) for 5 minutes. Changes of transient outward potassium channel (Ito) and steady state potassium channel (Iss) current intensity and corresponding current-voltage relationships were monitored. Results    After perfusing cardiac myocytes with anti-ADRβ1 in different concentrations for 5 minutes, current intensity and corresponding current-voltage relationships of Ito did not significantly chang (P>0.05).  Compared with current intensity of Iss (4.7±0.24) pA/pF at normal bath solution, Iss (3.6±0.18) pA/pF  decreased in 1/500 concentration of antiADRβ1 but without statistical significance, however, Iss  significantly decreased in 1/100 (3.5±0.18) pA/pF and 1/50 (3.1±0.15)pA/pF concentrations of anti-ADRβ1 in an obvious dose-dependent manner.  Conclusion    The aadrenoceptor β₁ Antibody inhibits Iss potassium channels of mouse cardiac myocytes but not Ito, which may play a role by stimulating β₁-adrenergic receptors. The results provide experimental basis for further investigation of the adrenoceptor β1 autoantibody in heart failure.

Key words: β₁-adrenoceptor; Antibody; Potassium channels; Cardiac myocytes; Mouse