Background: 

E-/R-type (Ca_v2.3) calcium channels are highly distributed in neuronal cells where they participate in neurotransmitter release and repetitive firing. Although expressed in the heart, their role is yet to be clarified. Our ongoing experiments aim at pin-pointing the actual role and molecular mechanism(s) of these pharmacoresistant voltage-gated Ca²⁺ channels in pacemaking and atrioventricular excitation conduction.

Methods: 

To shed more light on to the function of this channel in the heart, spontaneous activity of Ca_v2.3 knock out (KO) mouse hearts were assessed with the aid of the isolated perfused heart procedure (Langendorff technique), and the results compared with those from wild type mouse hearts. Heart activity was measured for about two hours and after a period of adaptation, three 15 second-periods within the first 40–45 minutes were selected for analysis.

Results: 

Generally, Ca_v2.3-deficient isolated perfused mouse hearts recorded a higher heart rate than control mice hearts (p < 0.01). There was however no significant difference in the coefficient of variation between both genotypes (p = 0.53). Most analyzed KO mouse hearts were more prone to exhibit pathophysiological parameters associated with excitation conduction disturbances, with the most prominent of them being the second and third-degree atrioventricular block.

Conclusions: 

Although detection of the E-/R-type calcium channels at protein level has so far been problematic, probably owing to the little quantity of protein expressed [1], their contributory role in heart rate regulation should not be overlooked. The present findings point towards a non negligible role of Ca_v2.3 calcium channels in excitation conduction in the mouse myocardium.