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Background  Glucagon-like peptide-1 (GLP-1) is a hormone predominately synthesized and secreted by intestinal L-cells. GLP-1 modulates multiple cellular functions and its receptor agonists are now used clinically for diabetic treatment. Interestingly, preclinical and clinical evidence suggests that GLP-1 agonists produce beneficial effects on dysfunctional hearts via acting on myocardial GLP-1 receptors. As the effects of GLP-1 on myocyte electrophysiology are largely unknown, this study was to assess if GLP-1 could affect the cardiac voltage-gated L-type Ca 2+  current (I Ca ).    Methods  The whole-cell patch clamp method was used to record I Ca  and action potentials in enzymatically isolated cardiomyocytes from adult canine left ventricles.    Results  Extracellular perfusion of GLP-1 (7-36 amide) at 5 nM increased I Ca  by 23 ± 8% ( p  < 0.05, n = 7). Simultaneous bath perfusion of 5 nM GLP-1 plus 100 nM Exendin (9-39), a GLP-1 receptor antagonist, was unable to block the GLP-1-induced increase in I Ca ; however, the increase in I Ca  was abolished if Exendin (9-39) was pre-applied 5 min prior to GLP-1 administration. Intracellular dialysis with a protein kinase A inhibitor also blocked the GLP-1-enhanced I Ca . In addition, GLP-1 at 5 nM prolonged the durations of the action potentials by 128 ± 36 ms ( p  < 0.01) and 199 ± 76 ms ( p  < 0.05) at 50% and 90% repolarization (n = 6), respectively.    Conclusions  Our data demonstrate that GLP-1 enhances I Ca  in canine cardiomyocytes. The enhancement of I Ca  is likely via the cAMP-dependent protein kinase A mechanism and may contribute, at least partially, to the prolongation of the action potential duration.

Glucagon-like peptide-1 enhances cardiac L-type Ca2+ currents via activation of the cAMP-dependent protein kinase A pathway