Glucagon‐like peptide‐1 (GLP‐1) is a hormone predominately synthesized and secreted by intestinal L cells. The biological effects of GLP‐1 are most likely via stimulation of GLP‐1 receptors. Animal studies have shown that GLP‐1 may protect the heart from ischemic damage and improve cardiac function in heart failure. However, the effects of GLP‐1 on myocyte electrophysiology have not been investigated. In this study we assessed the effects of GLP‐1 on cardiac action potentials. Extracellular application of GLP‐1 (7‐36) at 5 nM significantly prolonged the duration of action potentials in isolated canine ventricular myocytes. The duration at 50% repolarization was prolonged from 124 ± 24 ms for control to 252 ± 30 ms for GLP‐1 (n = 6, p < 0.01). Such prolongation accompanied with an increase in L‐type Ca2+ currents. Other parameters, such as amplitude, threshold, maximum upstroke velocity of action potentials, were not changed by GLP‐1. The effect of action potential prolongation was reversible after washout of GLP‐1. Lower concentrations (<0.05 nM) of GLP‐1 had no such effect. Adding GLP‐1 (7‐36) at 30 nM to a culture medium for 24 hours significantly increased the beating rate of cultured neonatal rat ventricular cells. Our data demonstrate that GLP‐1 prolongs cardiac action potential duration and increases beating rate of cardiomyocytes. These effects probably relate to GLP‐1‐induced increase in Ca2+ currents.