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Figure 1 | Cardiovascular Diabetology

Figure 1

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

Figure 1

Effects of GLP-1 on voltage-gated L-type Ca2+currents in isolated canine left ventricular myocytes. The representative traces of ICa in the absence (Control and Washout) and presence (GLP-1) of 5 nM GLP-1 are shown in panel A. The currents were evoked by the depolarizing pulses from the holding potential of -40 mV to 0 mV every 10 s. The current traces represented the ICa recorded at the times just before GLP-1 (Control), 12 min after GLP-1 perfusion (GLP-1), and 10 min after washout of GLP-1 (Washout). Panel B shows the average increase in the peak ICa in the presence of 5 nM GLP-1 (n = 7, p < 0.01). Panel C shows the effects of 5 nM GLP-1 on the current-voltage relationship of ICa recorded from a representative myocyte in the presence (solid circle) and absence (open circle) of 5 nM GLP-1. The normalized currents were calculated as the ratio of the peak ICa,GLP-1 to the maximal peak ICa,Control. The voltage protocol was composed of a group of pulses from -50 mV to 50 mV with 10 mV increments every 10 s. The membrane holding potential was -40 mV. The inset in the panel C shows the activation curves in the presence (solid circle) and absence (open circle) of 5 nM GLP-1. Panel D shows the steady-state inactivation of L-type Ca2+ currents (n = 7) in the presence (solid circle) and absence (open circle) of 5 nM GLP-1. The voltage protocol had double pulses consisting of a 200-ms test pulse to 0 mV following a 500-ms conditioning pulse varying from -60 to 20 mV in 10-mV increments every 10 ms with membrane holding potential of -40 mV. Normalized inactivation data were fit to a Boltzmann equation (solid lines): y = 1/{1 + exp[(V + V0.5)/K]}, where V0.5 is the voltage at which y = 0.5 and K is the slope factor.

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