Voltage-gated calcium channels (VGCCs) control the heart rate and rhythm in everyday life. VGCCs importantly contribute to the generation of sinoatrial node (SAN) automaticity and are key mediators of sympathetic and parasympathetic regulation of heart rate. In this chapter, we will review and comment on recent evidence showing that the expression of SAN VGCCs is endowed with intrinsic plasticity under different physiologic situations such as chronic physical training, ageing, and cardiac disease. In particular, it has been shown that the expression of L-type Cav1.3 and T-type Cav3.1 channels is downregulated in the SAN of trained animals, which contributes to the adaptation of heart rate to endurance training. Similarly, training induces a reduction in the expression of L-type Cav1.2 channels in the atrioventricular node (AVN), to adapt the impulse conduction velocity to a slower basal SAN rate associated with physical activity. Finally, expression of both L-type (ICaL) and T-type (ICaT) calcium currents is diminished in the ageing SAN, resulting in age-related bradycardia. The complex molecular network involved in the plasticity of VGCCs is mostly unexplored and will provide an exciting new research avenue in the field of excitability of cardiac myocytes.
Mesirca, P., Bidaud, I., Torre, E., Torrente, A., D'Souza, A., Mangoni, M. (2022). Functional Role and Plasticity of Voltage-Gated Calcium Channels in the Control of Heart Automaticity. In G.W. Zamponi, N. Weiss (a cura di), Voltage-Gated Calcium Channels (pp. 385-399). Springer International Publishing [10.1007/978-3-031-08881-0_13].
Functional Role and Plasticity of Voltage-Gated Calcium Channels in the Control of Heart Automaticity
Torre E.;
2022
Abstract
Voltage-gated calcium channels (VGCCs) control the heart rate and rhythm in everyday life. VGCCs importantly contribute to the generation of sinoatrial node (SAN) automaticity and are key mediators of sympathetic and parasympathetic regulation of heart rate. In this chapter, we will review and comment on recent evidence showing that the expression of SAN VGCCs is endowed with intrinsic plasticity under different physiologic situations such as chronic physical training, ageing, and cardiac disease. In particular, it has been shown that the expression of L-type Cav1.3 and T-type Cav3.1 channels is downregulated in the SAN of trained animals, which contributes to the adaptation of heart rate to endurance training. Similarly, training induces a reduction in the expression of L-type Cav1.2 channels in the atrioventricular node (AVN), to adapt the impulse conduction velocity to a slower basal SAN rate associated with physical activity. Finally, expression of both L-type (ICaL) and T-type (ICaT) calcium currents is diminished in the ageing SAN, resulting in age-related bradycardia. The complex molecular network involved in the plasticity of VGCCs is mostly unexplored and will provide an exciting new research avenue in the field of excitability of cardiac myocytes.
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