Abstract
Despite the large body of research on neural control of the heart, our quantitative understanding of the role of β-adrenergic receptor (β-AR) stimulation in human cardiac electrophysiology and arrhythmogenesis remains poor. One possible reason is in the fact that our knowledge is mostly based on experimental animal models (e.g., mouse and rabbit) characterized by quite different cellular electrophysiology. Indeed, we have shown that well conserved mammalian responses to β-AR stimulation (fight or flight) are mediated by different sub-cellular processes in mouse vs.
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