Stability of genetically engineered cardiac pacemaker - role of intracellular CA/sup 2+/ handling

Down-regulation of Kir2.1 channel reduces the inward-rectifier potassium current (i
_K1
), and transforms excitable ventricular myocytes to pacemaker cells. This provides a possible bio-technique to induce a biological pacemaker, as an alternative to an implantable electronic pacemaker. However there are two fundamental issues: (i) the stability of the pacemaker activity; (ii) the critical size of the biological pacemaker necessary for robust pacing and driving the surrounding ventricular muscle. In this study, we address the two issues by computer modelling