Mathematical simulations of ligand-gated and cell-type specific effects on the action potential of human atrium.

摘要: Abstract In the mammalian heart, myocytes and fibroblasts can communicate via gap junction, or connexin-mediated current flow. Some of effects this electrotonic coupling on action potential waveform human ventricular myocyte have been analyzed in detail. The present study employs a recently developed mathematical model atrial to investigate consequences heterogeneous cell–cell interaction atrium. Two independent physiological processes which alter physiology atrium studied. i) autonomic transmitter acetylcholine investigated by inclusion time-independent, acetylcholine-activated K + myocyte. ii) A non-selective cation is activated natriuretic peptides has incorporated into previously published cardiac fibroblast. These results identify subtle acetylcholine, arise from nonlinear interactions between ionic currents They also illustrate marked alterations arising fibroblast–myocyte source–sink principles when peptide-mediated conductance activated. Additional calculations simultaneous activation both these cell-type specific conductances within myocardium. This provides basis for beginning assess utility modeling understanding detailed complex paracrine environment